METHODS FOR TREATING RARE DISORDERS WITH ANTI-IL-6 THERAPY FIELD OF THE INVENTION The present invention relates to methods for treating rare histiocytic or lymphoproliferative disorders, in particular L- or C-group histiocytoses; and compositions for use in such methods. BACKGROUND TO THE INVENTION The histiocytoses are rare disorders characterized by the accumulation of macrophage, dendritic cell, or monocyte-derived cells in various tissues and organs of children and adults. More than 100 different subtypes have been described, with a wide range of clinical manifestations, presentations, and histologies. Their clinical behavior ranges from mild to disseminated and, sometimes, life-threatening forms. According to the revised “LCMRH” classification there are five general groups, as described in Emile JF et al, Revised classification of histiocytoses and neoplasms of the macrophage-dendritic cell lineages. Blood. 2016 Jun 2;127(22):2672-81. These are Langerhans-related (L), cutaneous and mucocutaneous (C), malignant histiocytoses (M), Rosai-Dorfman disease (R) and hemophagocytic lymphohistiocytosis and macrophage activation syndrome (H). Diagnosis is on the basis of clinical, radiographic, pathological, phenotypic, genetic, and/or molecular features. The rarity of the histiocytoses has meant that there are few guidelines on treatments, and a lack of effective therapies. Langerhans cell histiocytosis (LCH) of the L-group is the most common histiocytosis; its clinical and diagnostic characteristics and treatment options are reviewed in Tillotson CV, Anjum F, Patel BC. Langerhans Cell Histiocytosis. [Updated 2020 Dec 4]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK430885/. The disease has characteristics of both an abnormal reactive process and a neoplastic process. It may present initially as a rash. It can be disseminated and involve bone marrow, lungs, liver, spleen, lymph nodes, gastrointestinal (GI) tract, and the pituitary gland. Prognosis varies depending on presentation and organ involvement. Fluorodeoxyglucose (FDG) PET scanning is useful to assess patients with LCH and to monitor disease during treatment. Current therapies for LCH remain suboptimal, and are reviewed in Allen CE, Merad M, McClain KL. Langerhans-Cell Histiocytosis. N Engl J Med. 2018;379(9):856-868. Standard-of-care chemotherapy (vinblastine, prednisone, and mercaptopurine) fails to cure more than 50% of children with high-risk disease, and the majority of patients have long-term consequences, including a devastating neurodegenerative syndrome that can arise years after a patient is presumed to be cured. There is evidence that LCH is driven by pathologic MAPK activation in myeloid precursors, and there are reports that MAPK inhibition may show promise. Erdheim-Chester disease, a L-group histiocytosis, has a heterogeneous course and prognosis ranging from an asymptomatic process to a multi-systemic disease that can be life threatening (Diamone EL et al. Consensus guidelines for the diagnosis and clinical management of Erdheim- Chester Disease. Blood. 2014 Jul 24;124(4):483–492). The most common ECD manifestations include symmetric osteosclerosis of long bones, followed by retroperitoneal infiltration. ECD can involve several organ systems, including cardiovascular, pulmonary, neurologic, ophthalmologic, skin and musculoskeletal systems. First-line therapies for ECD include IFN-α, although it has limited efficacy and a poor side effect profile, and IL-1 inhibition with anakinra. Although C-group histiocytoses are now regarded as a separate classification, juvenile xanthogranuloma (JXG) and LCH were previously assigned to the same group of histiocytoses related to dendritic cells with variable biologic behaviour (Favara BE et al, Contemporary classification of histiocytic disorders. The WHO Committee On Histiocytic/Reticulum Cell Proliferations. Reclassification Working Group of the Histiocyte Society. Med Pediatr Oncol. 1997 Sep; 29(3):157-66). LCH and JXG show a clinical as well as a histopathological overlap, especially in children. In addition, a rare but well documented phenomenon of JXG developing in patients after treatment of LCH has been observed, raising questions as to the relatedness of LCH and JXG and to the pathogenesis of JXG (Strehl JD, Stachel KD, Hartmann A, Agaimy A. Juvenile xanthogranuloma developing after treatment of Langerhans cell histiocytosis: case report and literature review. Int J Clin Exp Pathol. 2012;5(7):720-725). Clinical and diagnostic characteristics and treatment options for XJG are reviewed in Collie JS, Harper CD, Fillman EP. Juvenile Xanthogranuloma. [Updated 2020 Aug 10]. In: StatPearls [Internet]. Treasure Island (FL): StatPearls Publishing; 2020 Jan-. Available from: https://www.ncbi.nlm.nih.gov/books/NBK526103/. Typically, the clinical presentation consists of solitary or multiple yellow-orange-brown firm papules or nodules. The most common locations are the face, neck, and upper torso. Cutaneous lesions are usually asymptomatic, and most lesions spontaneously involute over the course of several years. Although occurring rarely, ocular involvement is the most common extracutaneous site involved, followed by the lungs. Management of non-cutaneous (internal) lesions may include any combination of surgery, chemotherapy, radiotherapy, and immunosuppression. Interleukin-6 (IL-6) is a pro-inflammatory cytokine, and is known to signal through the JAK/STAT pathway (Harrison DA. The Jak/STAT pathway. Cold Spring Harb Perspect Biol. 2012;4(3):a011205). There are at least two major biological functions of IL-6: mediation of acute phase proteins and acting as a differentiation and activation factor (Avvisti, G. et al., Baillieres Clinical Hematology 8: 815-829 (1995) and Poli, V. et al., EMBO 13: 1189-1196 (1994). Dysregulated IL-6 expression is an established driver for symptomatology and pathogenesis of the lymphoproliferative disorder idiopathic multicentric Castleman disease (iMCD), which is characterised by multicentric lymphadenopathy, with systemic inflammation, cytopenias and life-threatening multiple organ dysfunction resulting from a cytokine storm, as discussed in Fajgenbaum DC (2018) Novel insights and therapeutic approaches in idiopathic multicentric Castleman disease. Blood. 132(22):2323-2330. IL-6 is implicated in pathogenesis of other lymphoproliferative disorders, in addition to iMCD, including high-grade B-cell lymphomas (Emilie D et al. Interleukin-6 production in high-grade B lymphomas: correlation with the presence of malignant immunoblasts in acquired immunode¿ciency syndrome and in human immunode¿ciency virus-seronegative patients. Blood.1992;80:498-504) and myelomas (Klein B, Zhang X, Lu Z, Bataille R. Interleukin-6 in human multiple myeloma. Blood. 1995;85:863-872). IL-6 is also implicated in pathogenesis of the histiocytic disorder Rosai- Dorfman disease (Aouba A et al. Dramatic clinical efficacy of cladribine in Rosai-Dorfman disease and evolution of the cytokine profile: towards a new therapeutic approach. Haematologica.2006 Dec;91(12 Suppl):ECR52). It has been shown that IL-6 levels were markedly elevated in patients with ECD, as described in Arnaud L, Gorochov G, Charlotte F, et al. Systemic perturbation of cytokine and chemokine networks in Erdheim-Chester disease: A single-center series of 37 patients. Blood. 2011 Mar 10;117(10):2783–2790. IL-6 gene expression has been detected in reactive cells of LCH in patient tissue samples (Foss HD et al. Monokine expression in Langerhans' cell histiocytosis and sinus histiocytosis with massive lymphadenopathy (Rosai-Dorfman disease). J Pathol. 1996 May;179(1):60-5. A wide range of other cytokines are abundantly expressed in LCH lesions, which may create a cytokine storm (Egeler RM et al. Differential In situ cytokine profiles of Langerhans-like cells and T cells in Langerhans cell histiocytosis: abundant expression of cytokines relevant to disease and treatment. Blood. 1999 Dec 15;94(12):4195-201). Siltuximab is a chimeric (human-murine) immunoglobulin G1k (IgG1k) monoclonal antibody having a binding specificity for human IL-6, and is produced in a Chinese hamster ovary (CHO) cell line by recombinant DNA technology. It is described in European Public Assessment Report (EPAR) of the Committee for Medicinal Products for Human Use (CHMP) of the European Medicines Agency (EMA) for Sylvant® (EMEA/H/C/003708, last updated 8 October 2019), and in WO 2004/039826A1. Siltuximab is authorised in USA, European Union and elsewhere for treatment of idiopathic Multicentric Castleman’s Disease (iMCD) for patients who are human immunodeficiency virus (HIV) negative and human herpesvirus-8 (HHV-8) negative. The recommended treatment regimen for iMCD is 11 mg/kg siltuximab given over 1 hour as an intravenous infusion administered every 3 weeks until treatment failure. There remains a need for effective treatments for L-group and C-group histiocytoses. The listing or discussion of an apparently prior-published document in this specification should not necessarily be taken as an acknowledgement that the document is part of the state of the art or is common general knowledge. SUMMARY OF THE INVENTION A first aspect of the invention provides an antibody or fragment thereof which is capable of inhibiting human IL-6 for use in a treatment regimen for treating L-group or C-group histiocytosis in a patient. A corresponding aspect of the invention provides a method of treating L-group or C-group histiocytosis in a patient, comprising administering an antibody or fragment thereof which is capable of inhibiting human IL-6. DESCRIPTION OF THE FIGURES Figure 1. Clinical trial study design. DETAILED DESCRIPTION OF THE INVENTION The present invention provides a method of treating a L-group or C-group histiocytosis in a patient, and compositions for use in the method. The present invention is based on a clinical trial of siltuximab in the treatment of various rare IL-6-associated histiocytosis or lymphoproliferative disorders, including the presently described indication. In devising the clinical trial, the inventors postulated that data from patients having different histiocytosis or lymphoproliferative disorders could be considered together because all of the disorders covered by the study may be associated with elevated serum IL-6, and all patients eligible to be enrolled in the trial must exhibit elevated serum IL-6. The inventors therefore decided to select for the clinical trial various disorders not normally grouped together. By “IL-6-associated” histiocytic or lymphoproliferative disorder, we include the meaning that elevated IL-6, particularly serum IL-6, has been detected in the type of disease in question. By “histiocytic disorder” or “histiocytosis”, we mean a disorder characterized by the accumulation of macrophage, dendritic cell, or monocyte-derived cells, as described in Emile JF et al, Revised classification of histiocytoses and neoplasms of the macrophage-dendritic cell lineages. Blood. 2016 Jun 2;127(22):2672-81. By “lymphoproliferative disorder”, we mean a disorder characterized by uncontrolled production of lymphocytes that cause lymphocytosis and lymphadenopathy. They may involve various immunophenotypes of T, B, and NK cells. Analysis of blood samples frequently reveals large quantities of immature lymphocytes that are usually oligoclonal. Lymphoproliferative disorders include lymphoid neoplasms and non-malignant lymphoproliferative disorders. Lymphoid neoplasms may be classified and diagnosed according to the 2016 revision of the World Health Organization (WHO) classification of lymphoid neoplasms, as described in Swerdlow SH et al. The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood. 2016 May 19;127(20):2375-90. Classification and diagnosis of histiocytoses are described in Emile JF et al, Revised classification of histiocytoses and neoplasms of the macrophage-dendritic cell lineages. Blood. 2016 Jun 2;127(22):2672-81. The L-group includes LCH, ECD, supported by both diseases have clonal mutations involving genes of the MAPK pathway in >80% of cases. The L-group also includes Mixed ECD and LCH, and indeterminate cell histiocytosis (ICH), as shown in Table 1. Table 1: Histiocytoses of the L group Disease Subtypes Disease Subtypes ECD ECD classical type ECD without bone involvement Associated with another myeloproliferative/myelodysplastic disorder Extracutaneous or disseminated JXG with MAPK-activating mutation or ALK translocations Mixed ECD and LCH ECD, Erdheim-Chester disease; ICH, indeterminate cell histiocytosis; LCH, Langerhans cell histiocytosis; MS, multiple system; RO, risk organ; SS, single system. The diagnosis of LCH is based on clinical and radiological findings in combination with histopathological analyses identifying tissue infiltration by histiocytes with ultrastructural or immunophenotypic characteristics of Langerhans cells (LCs). These are positive for CD1a and CD207 expression in LCH, whereas in ICH the LCs are CD207 negative. Diagnosis of ECD is made with histology and phenotype of histiocytes in appropriate clinical and radiological context. Skeletal involvement occurs in >95% of ECD patients. Bilateral, symmetric cortical osteosclerosis of the diaphyseal and metaphyseal regions is highly suggestive of ECD,28 and positron emission tomography (PET) with 18F-labeled fluorodeoxyglucose (PET–computed tomography [CT]) has a high specificity. ECD histiocytes are positive for CD68 and CD163 and negative for CD1a. Some histiocytes may be positive for S100 protein. 20% of patients with ECD also have LCH lesions. all extracutaneous or disseminated JXG with gain-of-function mutation of BRAF, NRAS, KRAS, or MAP2K1 is classed as ECD. The C-group comprises cutaneous and mucocutaneous histiocytoses, also referred to as non- LCH of skin and mucosa, as shown in Table 2. Table 2: Non-LCH of skin and mucosa (C group) Cutaneous non-LCH histiocytoses XG family JXG AXG SRH Cutaneous non-LCH histiocytoses t eralized eruptive histiocytosis; JXG, juvenile xanthogranuloma; MRH, multicentric reticulohistiocytosis; NXG, necrobiotic xanthogranuloma; PNH, progressive nodular histiocytosis; RDD, Rosai-Dorfman disease; SRH, solitary reticulohistiocytoma; XD, xanthoma disseminatum; XG, xanthogranuloma. The C-group includes the xanthogranuloma (XG) family. The various diseases included in this family can be defined by the clinical setting, that is, solitary, multiple, or disseminated, the areas of the body involved and the age of the patient. JXG is the commonest of the non-LCH. Histologically, JXG/AXG/SRH appear as well-circumscribed dermal or dermohypodermal nodules sparing the epidermis. Mature lesions contain foamy cells, foreign-body giant cells, and Touton cells as well as macrophages, lymphocytes, and eosinophils. Older, regressing lesions show proliferation of fibroblasts and fibrosis that replace part of the infiltrate. The non-XG family includes various rare disorders. Patients for whom the treatment regimen of the invention is intended may have a L-group or C-group histiocytosis. The L-group histiocytosis may be any of Erdheim-Chester disease (ECD), Langerhans cell histiocytosis (LCH), mixed ECD and LCH or Indeterminate cell histiocytosis (ICH). The C-group histiocytosis may be any of the xanthogranuloma family, namely juvenile xanthogranuloma (JXG), adult xanthogranuloma (AXG), solitary reticulohistiocytoma (SRH), benign cephalic histiocytosis (BCH), generalized eruptive histiocytosis (GEH), progressive nodular histiocytosis (PNH), or xanthoma disseminatum (XD); or any of the non- xanthogranuloma family, namely cutaneous Rosai-Dorfman disease, necrobiotic xanthogranuloma (NXG), cutaneous histiocytoses not otherwise specified, or multicentric reticulohistiocytosis (MRH). The C-group histiocytoses may be a cutaneous non-LCH histiocytosis without a major systemic component; or a cutaneous non-LCH histiocytoses with a major systemic component. Typically, the patient is negative for infection with HIV, HHV-8, or EBV. These viruses may produce viral IL-6. Siltuximab and other IL-6 antibodies bind human but not viral IL-6. However, EBV infection is common, and may be latent in patients. EBV may not be relevant to the pathology to be treated. Thus, the treatment may be appropriate for patients who have EBV infection. Similarly, HIV or HHV-8 may not be relevant to the pathology to be treated, so the anti-IL-6 treatment may still be appropriate for patients who have HIV or HHV-8 infection. Typically, the patient is negative for infection with HIV and HHV-8. Diagnosis of HIV, HHV-8 or EBV can be performed by serological analysis or PCR, as known in the art. A patient having a disease of a type that may have elevated IL-6 may be considered to have an IL-6-associated disease and be suitable for the treatment of the invention. Typically, the patient will be assessed for elevated levels of IL-6 and/or C-reactive protein (CRP), its qualified surrogate, to identify that the particular patient’s disease is IL-6-associated. . Thus, “IL-6- associated” also includes the meaning that the specific patient has elevated IL-6 and/or CRP levels, typically elevated serum IL-6 and/or CRP levels. Circulating IL-6 levels can be expected to correlate with IL-6 levels at the site of disease. The treatment regimen of the present invention is particularly suitable for patients for which excessive IL-6 is suspected to be contributing to pathology, i.e., “IL-6-driven disease”. IL-6 is the primary inducer of CRP synthesis in the liver (Heinrich PC et al, Interleukin-6 and the acute phase response. Biochem J 1990.265(3):621–636). CRP suppression has previously been used as a surrogate for inhibition of IL-6 signaling (Puchalski T et al, Pharmacokinetic and pharmacodynamic modeling of an antiinterleukin-6 chimeric monoclonal antibody (siltuximab) in patients with metastatic renal cell carcinoma. Clin Cancer Res. 2010. 16(5):1652–1661). Patients for which the treatment regimen of the present invention may be particularly suitable may have elevated serum IL-6 concentration (such as a serum IL-6 concentration above upper limit of normal for the testing laboratory, typically >6 pg/mL) and/or elevated serum CRP concentration (such as serum CRP above upper limit of normal for the testing laboratory, typically >10 mg/L). A normal range of serum IL-6 for a healthy person is <5 pg/mL. Patients for whom IL-6 is suspected of contributing to pathology may have serum IL-6 levels at diagnosis >5 pg/mL or >6 pg/mL. In such patients, the disease may be regarded as “IL-6-associated”. Serum IL-6 levels in patients having an IL-6-associated histiocytic or lymphoproliferative disorder may be in the range of 7 pg/mL to 10 ng/mL or greater. In primary T cell lymphoma (PTCL), a serum IL-6 concentration as high as about 3 ng/mL has been observed (Raziuddin et al (1994) Cancer 73:2426-31). A normal range of serum CRP for a healthy person is from 0.3 to 10 mg/L. Patients for whom IL-6 is suspected of contributing to pathology, i.e., “IL-6-associated” disease may have serum CRP levels at diagnosis >10 mg/L. Although serum CRP can rise 1000-fold or more from healthy levels in response to injury, inflammation, or tissue death, a level greater than 100 mg/L strongly suggests bacterial infection, according to Chandrashekara S. (2014) Internet J Rheumatol and Clin Immunol 2(S1): SR3. Serum CRP levels in patients having an IL-6- associated histiocytic or lymphoproliferative disease are typically in the range of 11 mg/L to 100 mg/L, but could be greater than 100 mg/L. It may be necessary to exclude bacterial infection in cases of very high serum CRP levels. Thus, the patient typically has a serum IL-6 concentration of >6 pg/mL and/or a serum CRP concentration of >10 mg/L prior to commencing the treatment regimen, typically within one month prior to commencing the treatment regimen. CRP is typically monitored periodically during the treatment regimen, rather than serum IL-6, because measurement of free serum IL-6 levels will likely be confounded by IL-6 antibody therapy, as presently available IL-6 diagnostic tests are unable to distinguish free from antibody-bound IL-6. IL-6 and CRP may be measured using commercially available enzyme- linked immunosorbent assay (ELISA) kits (e.g. from R&D Systems, Minneapolis, MN), and other methods known in the art. The antibody or fragment thereof for use of the invention is capable of inhibiting human IL-6. IL-6 can bind to the IL-6 receptor (IL-6R) expressed on mitogen-activated B cells, T cells, peripheral monocytes, and certain tumors (Ishimi, Y. et al., J. Immunology 145: 3297-3303 (1990)). IL-6R has at least two different components and is composed of an alpha chain called gp80, also referred to as soluble IL-6R, that is responsible for IL-6 binding and a cell-membrane bound beta chain designated gp130 that is needed for signal transduction (Adebanjo, O. et al., J. Cell Biology 142: 1347-1356 (1998) and Poli, V. et al., EMBO 13: 1189-1196 (1994)). An antibody which is capable of inhibiting human IL-6 must be capable of specifically binding to human IL-6, and of inhibiting its interaction with gp80 (IL-6R) or otherwise preventing gp130 activation. By “capable of specifically binding”, we include the ability of the antibody or antigen- binding fragment to bind at least 10-fold more strongly to the relevant polypeptide, e.g. IL-6, than to any other polypeptide; preferably at least 50-fold more strongly and more preferably at least 100-fold more strongly. By “inhibiting”, we include “neutralising”. Inhibitory antibodies to IL-6 can typically be divided into two groups; and the putative epitopes on the IL-6 molecule designated Site I and Site II. Site I binders prevent binding to the gp80 (IL-6R) and thereby prevent gp130 activation. The Site I epitope was further characterized as comprising regions of both amino terminal and carboxy terminal portions of the IL-6 molecule. Site II-binders prevent gp130 activation and therefore may recognize a conformational epitope involved in signalling. Binding of the antibody may be measured by surface plasmon resonance, for example, by immobilizing the antibody on a chip and using recombinant human IL-6 as analyte, as described in WO 2004/039826A1. Suitable antibodies may bind IL-6 with an affinity (Kd) of at least 10 ^-9 M, preferably at least 10 ^-10 M, preferably at least 10 ^-11 or 5 x 10 ^-11 M. Epitope mapping to identify Site I or Site II binders may be performed by binding to human IL-6-mutant proteins as described in Brakenhoff, J. et al. (1990) J. Immunology 145: 561-568). Inhibition of IL-6 activity may be measured by assaying proliferation of the murine B myeloma cell line, 7TD1, in response to IL-6, as described in WO 2004/039826A1. Suitable antibodies may inhibit >50%, such as >90%, such as substantially 100% of 7TD1 cell proliferation in response to IL-6. By “IL-6” we include any natural or synthetic protein with structural and/or functional identity to the human IL-6 protein, such as defined UniProt Accession No. P05231, or natural variants thereof. IL-6 gene and/or amino acid sequences are disclosed in Eur. J. Biochem (1987) 168, 543-550; J. Immunol. (1988)140, 1534-1541; and Agr. Biol. Chem. (1990)54, 2685-2688. By “antibody” we include substantially intact antibody molecules, as well as chimaeric antibodies, humanised antibodies, human antibodies (wherein at least one amino acid is mutated relative to the naturally occurring human antibodies), single chain antibodies, bi- specific antibodies, antibody heavy chains, antibody light chains, homo-dimers and heterodimers of antibody heavy and/or light chains, and antigen binding fragments and derivatives of the same. The term also includes antibody-like molecules which may be produced using phage-display techniques or other random selection techniques for molecules. The term also includes all classes of antibodies, including IgG, IgA, IgM, IgD, and IgE. Also included for use in the invention are antibody fragments such as Fab, F(ab’)2, Fv, Fab’, scFv (single-chain variable fragment), or di-scFv and other fragments thereof that retain the antigen-binding site. Similarly, the term “antibody” includes genetically engineered derivatives of antibodies such as single-chain Fv molecules (scFv) and single-domain antibodies (dAbs). Preferred antibodies are chimaeric, such as mouse-human chimaeric antibodies, CDR-grafted antibodies, humanised antibodies, or human antibodies. Although the antibody may be a polyclonal antibody, it is preferred if it is a monoclonal antibody, or that the antigen-binding fragment is derived from a monoclonal antibody. Suitable monoclonal antibodies may be prepared by known techniques, for example those disclosed in “Monoclonal Antibodies; A manual of techniques”, H Zola (CRC Press, 1988) and in “Monoclonal Hybridoma Antibodies: Techniques and Application”, SGR Hurrell (CRC Press, 1982). The antibodies may be human antibodies in the sense that they have the amino acid sequence of human antibodies with specificity for the IL-6; however, it will be appreciated that they may be prepared using methods known in the art that do not require immunisation of humans. Suitable antibodies may be prepared from transgenic mice which contain human immunoglobulin loci, as described in Lee, E., Liang, Q., Ali, H. et al. Complete humanization of the mouse immunoglobulin loci enables efficient therapeutic antibody discovery. Nat Biotechnol 32, 356–363 (2014). https://doi.org/10.1038/nbt.2825. Suitably prepared non-human antibodies can be “humanised” in known ways, for example, by inserting the CDR regions of mouse antibodies into the framework of human antibodies. Chimeric antibodies are discussed by Neuberger et al (1998, 8th International Biotechnology Symposium Part 2, 792-799). It will be appreciated by persons skilled in the art that the binding specificity of an antibody or antigen-binding fragment thereof is conferred by the presence of complementarity determining regions (CDRs) within the variable regions of the constituent heavy and light chains. As discussed below, in a particularly preferred embodiment of the antibodies and antigen-binding fragments, binding specificity for IL-6 is conferred by the presence of one or more and typically all six of the CDR amino acid sequences defined herein. Preferably, the antibody or antigen-binding fragment comprises an antibody Fc region. It will be appreciated by the skilled person that the Fc portion may be from an IgG antibody, or from a different class of antibody (such as IgM, IgA, IgD, or IgE). For example, the Fc region may be from an IgG1, IgG2, IgG3, or IgG4 antibody. Advantageously, however, the Fc region is from an IgG1 antibody. It is preferred that the antibody or antigen-binding fragment is an IgG molecule, or is an antigen-binding fragment or variant of an IgG molecule. Suitable antibodies and fragments are described in WO 2004/039826A1. Suitably, the antibody or fragment is a chimeric, humanized or CDR grafted antibody or fragment thereof comprising a heavy chain variable region in which CDR1, CDR2, and CDR3 comprise the amino acid sequences SEQ ID NO: 1, SEQ ID NO: 2 and SEQ ID NO: 3, respectively; and a light-chain variable region in which CDR1, CDR2, and CDR3 comprise the amino acid sequences SEQ ID NO: 4, SEQ ID NO: 5 and SEQ ID NO: 6, respectively, and a constant region derived from a human IgG antibody. VH CDR1 Ser Phe Ala Met Ser (SEQ ID NO. 1) VH CDR2 Glu Ile Ser Ser Gly Gly Ser Tyr Thr Tyr Tyr Pro Asp Thr Val Thr Gly (SEQ ID NO. 2) VH CDR3 Gly Leu Trp Gly Tyr Tyr Ala Leu Asp Tyr (SEQ ID NO. 3) VL CDR1 Ser Ala Ser Ser Ser Val Ser Tyr Met Tyr (SEQ ID NO. 4) VL CDR2 Asp Thr Ser Asn Leu Ala Ser (SEQ ID NO. 5) VL CDR3 Gln Gln Trp Ser Gly Tyr Pro Tyr Thr (SEQ ID NO. 6) In a preferred embodiment the antibody is siltuximab, or an antigen-binding fragment thereof. Siltuximab, also known as CNTO328 and CLLB8, with the US FDA UNII Identifier T4H8FMA7IM and the WHO ATC code L04AC11 is a chimeric (human-murine) IgG1k monoclonal antibody that binds to human IL-6. The intact molecule contains 1324 amino acid residues and is composed of two identical heavy chains (approximately 50 kDa each) and two identical light chains (approximately 24 kDa each) linked by inter-chain disulfide bonds. Siltuximab contains the antigen-binding variable region of the murine antibody, CLB-IL-6-8, and the constant region of a human IgG1k immunoglobulin. The complete amino acid sequences of the heavy and light chains of siltuximab are shown below. SEQ ID NO. 7 Siltuximab heavy chain amino acid sequence EVQLVESGGKLLKPGGSLKLSCAASGFTFSSFAMSWFRQSPEKRLEWVAEISSGGSYTYY PDTVTGRFTISRDNAKNTLYLEMSSLRSEDTAMYYCARGLWGYYALDYWGQGTSVTVSSA STKGPSVFPLAPSSKSTSGGTAALGCLVKDYFPEPVTVSWNSGALTSGVHTFPAVLQSSG LYSLSSVVTVPSSSLGTQTYICNVNHKPSNTKVDKKVEPKSCDKTHTCPPCPAPELLGGP SVFLFPPKPKDTLMISRTPEVTCVVVDVSHEDPEVKFNWYVDGVEVHNAKTKPREEQYNS TYRVVSVLTVLHQDWLNGKEYKCKVSNKALPAPIEKTISKAKGQPREPQVYTLPPSRDEL TKNQVSLTCLVKGFYPSDIAVEWESNGQPENNYKTTPPVLDSDGSFFLYSKLTVDKSRWQ QGNVFSCSVMHEALHNHYTQKSLSLSPGK SEQ ID NO. 8 Siltuximab light chain amino acid sequence QIVLIQSPAIMSASPGEKVTMTCSASSSVSYMYWYQQKPGSSPRLLIYDTSNLASGVPVR FSGSGSGTSYSLTISRMEAEDAATYYCQQWSGYPYTFGGGTKLEIKRTVAAPSVFIFPPS DEQLKSGTASVVCLLNNFYPREAKVQWKVDNALQSGNSQESVTEQDSKDSTYSLSSTLTL SKADYEKHKVYACEVTHQGLSSPVTKSFNRGEC Siltuximab and methods of preparing it, including by recombinant expression of encoding nucleic acid sequences, are described in WO 2004/039826A1. Other suitable antibodies include olokizumab, which is a IgG4k antibody humanized from rat, and is described in Shaw, S., Bourne, T., Meier, C., Carrington, B., Gelinas, R., & Henry, A., et al. (2014). Discovery and characterization of olokizumab. mAbs, 6(3), 773-781; elsilimomab (also known as B-E8), which is a mouse IgG1k monoclonal antibody described in Wijdenes J, Clement C, Klein B, et al. Human recombinant dimeric IL-6 binds to its receptor as detected by anti-IL-6 monoclonal antibodies. Mol Immunol. 1991;28(11):1183–1192; or the human monoclonal antibody clone 1339 derived from elsilimomab as described in Fulciniti, M., Hideshima, T., Vermot-Desroches, C., Pozzi, S., Nanjappa, P., Shen, Z.,. & Tai, Y. T. (2009). A high-affinity fully human anti–IL-6 mAb, 1339, for the treatment of multiple myeloma. Clinical Cancer Research, 15(23), 7144-7152. Further suitable antibodies include clazakizumab (formerly ALD518 and BMS-945429), which is an aglycosylated, humanized rabbit IgG1 monoclonal antibody against interleukin-6, described in Mease PJ, Gottlieb AB, et al. (September 2016). "The efficacy and safety of clazakizumab, an anti-interleukin-6 monoclonal antibody, in a phase IIb study of adults with active psoriatic arthritis". Arthritis Rheumatol. 68 (9): 2163– 73; sirukumab, which is a human monoclonal IgG1 kappa antibody described in Smolen JS, Weinblatt ME, Sheng S, Zhuang Y, Hsu B. Sirukumab, a human anti-interleukin-6 monoclonal antibody: a randomised, 2-part (proof-of-concept and dose-finding), phase II study in patients with active rheumatoid arthritis despite methotrexate therapy. Ann Rheum Dis. 2014 Sep;73(9):1616-25. doi: 10.1136/annrheumdis-2013-205137. Epub 2014 Apr 3. PMID: 24699939; PMCID: PMC4145446. Further suitable antibodies include the MH166 antibody (Matsuda, T. et al., Eur. J. Immunol. (1988) 18, 951-956) and the SK2 antibody (Sato, K. et al., The abstracts of the 21st Annual Meeting of the Japanese Society for Immunology (1991) 21, 166). Fragments of any of these antibodies may also be used. The antibody or fragment may be administered by at least one mode selected from parenteral, subcutaneous, intramuscular, intravenous, intrarticular, intrabronchial, intraabdominal, intracapsular, intracartilaginous, intracavitary, intracelial, intracelebellar, intracerebroventricular, intracolic, intracervical, intragastric, intrahepatic, intramyocardial, intraosteal, intrapelvic, intrapericardiac, intraperitoneal, intrapleural, intraprostatic, intrapulmonary, intrarectal, intrarenal, intraretinal, intraspinal, intrasynovial, intrathoracic, intrauterine, intravesical, bolus, vaginal, rectal, buccal, sublingual, intranasal, or transdermal. Suitable formulations for these routes of administration are described in WO 2004/039826. The antibody or fragment is administered in an effective amount. The antibody or fragment can be administered as a one-time or periodic dosage of 0.1 to 100 mg/kg, such as 0.5, 0.9, 1.0, 1.1, 1.5, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 40, 45, 50, 60, 70, 80, 90 or 100 mg/kg, per day, on at least one day of a treatment regimen, such as on day 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, or 40, where day 1 is the start of treatment; or on week 1, 2, 3, 4, 5, 6, 7, 8, 9, 10, 11, 12, 13, 14, 15, 16, 17, 18, 19, 20, 21, 22, 23, 24, 25, 26, 27, 28, 29, 30, 31, 32, 33, 34, 35, 36, 37, 38, 39, 40, 41, 42, 43, 44, 45, 46, 47, 48, 49, 50, 51, or 52 of treatment, using single, infusion or repeated doses. Suitably, the treatment regimen comprises at least one first intensity treatment cycle comprising intravenously administering the antibody at a first antibody treatment density, or the fragment at an equivalent fragment treatment density having an equivalent antagonistic effect on human IL-6. By “treatment density”, we mean the cumulative dose divided by the total duration of antibody therapy at the specified intensity. The “treatment density” is expressed as a dose in mg/kg per time interval. The time interval may or may not be of the same duration as a treatment cycle. Treatment density is conveniently expressed in terms of dose over a three-week interval. However, it is envisaged that the antibody therapy at a specified intensity may occur over a shorter duration than three weeks, and therefore, a corresponding treatment density is also defined over a shorter interval. In particular, a treatment density of >11 mg/kg per 3-week interval is equivalent to 11 mg/kg per < 3-week interval. The dose of the antibody or fragment is determined according to the weight in kg of the patient. An antibody fragment is to be administered at an equivalent fragment treatment density having an equivalent antagonistic effect on human IL-6 to the whole antibody from which the fragment is derived. The equivalent fragment treatment density may be calculated according to the fragment molecular weight compared to the molecular weight of the whole antibody, also referred to as parent antibody. For example, if a given antibody has a molecular weight of 150 kD, and a Fab fragment has a molecular weight of 50 kD, then a fragment dose that is one third of the antibody dose should provide an equivalent antagonistic effect on human IL-6. Thus, if the antibody treatment density was 12 mg/kg per three-week interval, then the equivalent fragment treatment density for the Fab fragment would be 4 mg/kg per three-week interval. The equivalent antagonistic effect on human IL-6 may also be determined according to the amount of human IL-6 that the fragment can specifically bind to, compared to the amount of human IL-6 that the parent antibody can specifically bind to. These amounts may be determined by various assays, including ELISA. The term “treatment cycle” as used herein means a course of one or more treatments or treatment periods that is repeated on a regular schedule and may encompass a period of rest. For example, a treatment given one day followed by 20 days of rest is 1 treatment cycle of 21 days. The treatment cycle may be repeated, either identically or in an amended form, e.g., with a different dose or schedule, or with different additional treatments. A “treatment interval” is the interval between starting and completing a treatment cycle. By “first intensity treatment cycle”, we mean a treatment cycle characterised by the specified treatment density. Second and third intensity treatment cycles are to be understood accordingly, as meaning a treatment cycle characterised by the specified treatment density. The “overall treatment time” means the time period comprising all treatment cycles. As described above, treatment cycles may comprise time periods of no treatment (intervals in which no treatment is administered to the patient, i.e., no antibody, no other drug). Thus, as used herein, the overall treatment time may also comprise said intervals of no treatment within treatment cycles. A “treatment period” with a specific preparation or treatment as used herein means the period of time in which said specific preparation or treatment is administered to the patient. For example, if an antibody is administered for 1 hour, and there are no further administrations in the subsequent 20 days, then the treatment period with the antibody is 1 hour. The patient is administered the antibody for at least one first intensity treatment cycle. The number of first intensity treatment cycles may be one or more than one, such as 2, 3, 4, 5, up to 10 or more, or up to 20 more. After the first treatment cycle at the first intensity, the patient may either continue to receive more treatment cycles at the first intensity, or be treated with at least one treatment cycle at an increased intensity, or discontinue antibody therapy. If the patient obtains clinical benefit after receiving one or more treatment cycles at the first intensity, the patient will typically continue with further treatment cycles at that intensity, unless and until further dose escalation is clinically indicated. Further dose escalation may be considered if the patient’s disease progresses, or if the response to treatment is suboptimal, as discussed further below. However, if the patient experiences unacceptable toxicity or clinical deterioration during treatment at the first intensity, further dose escalation would typically not be attempted. The decision whether to continue at the same treatment density, escalate to a higher treatment density, or discontinue antibody therapy will generally be the responsibility of the treating physician, taking into account the patient’s response to and toleration of antibody therapy at the current treatment density as well as serum CRP levels. Typically, according to the treatment regimen of the invention, the first antibody treatment density is ≥ 5 mg/kg per three-week interval, such as ≥ 6 mg/kg, such as ≥ 7 mg/kg, such as ≥ 8 mg/kg, such as ≤ 9 mg/kg, such as ≥ 10 mg/kg such as ≤ 11 mg/kg per three-week interval; or ≤ 5 mg/kg per < three-week interval. A treatment density of ≤ 5 mg/kg per ≤ 3- week interval may include any of the above treatment densities, typically to the nearest mg/kg, wherein the time interval is expressed as less than 3 weeks, for example wherein the time interval is 20 days, 15 days, 14 days, 10 days, or 7 days. In one embodiment, the first antibody treatment density is 11 ± 5, 4, 3, 2, or 1 mg/kg per three-week interval, such as 11 mg/kg per three-week interval; or 8 ± 3, 2, or 1 mg/kg per two-week interval, such as 8 mg/kg per two-week interval; or 4 ± 2, or 1 mg/kg per one-week interval, such as 4 mg/kg per one-week interval. The expression X ± Y is intended to cover the full range of doses within the limits of X ± Y. Hence 11 ± 5, 4, 3, 2, or 1 mg/kg refers to the ranges of 6 to 16, 7 to 15, 8 to 14, 9 to 13, or 10 to 12 mg/kg. The equivalent fragment treatment density would be determined as explained above. These treatment densities correspond to the standard treatment density for siltuximab in the treatment of iMCD, which is 11 mg/kg per three-week interval. In another embodiment, the first antibody treatment density is 22 ± 5, 4, 3, 2, or 1 mg/kg per three-week interval, or 33 ± 5, 4, 3, 2, or 1 mg/kg per three-week interval or 44 ± 5, 4, 3, 2, or 1 mg/kg per three-week interval, such as wherein the first antibody treatment density is 22, 33 or 44 mg/kg per three-week interval; or 15 ± 3, 2, or 1 mg/kg per two-week interval, or 22 ± 3, 2, or 1 mg/kg per two-week interval, or 29 ± 3, 2, or 1 mg/kg per two-week interval; or 7 ± 2, or 1 mg/kg per one-week interval, or 11 ± 2, or 1 mg/kg per one-week interval, or 15 ± 2, or 1 mg/kg per one-week interval. These treatment densities correspond to multiples of the standard treatment density for siltuximab in the treatment of iMCD. In one embodiment of the invention, after the patient has been treated with the at least one first intensity treatment cycle, the patient is treated with at least one second intensity treatment cycle comprising intravenously administering the antibody in a second antibody treatment density or equivalent fragment density, if clinically indicated; wherein the second antibody treatment density is greater than the first antibody treatment density. Suitably, (a) if the first antibody treatment density is 11 ± 5 mg/kg per three-week interval, or 8 ± 3 mg/kg per two-week interval, or 4 ± 2 mg/kg per one-week interval, then the second antibody treatment density is: 22 ± 5 mg/kg per three-week interval, or 15 ± 3 mg/kg per two- week interval, or 7 ± 2 mg/kg per one-week interval; or 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval; or 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two-week interval, or 15 ± 2 mg/kg per one-week interval; or (b) if the first antibody treatment density is 22 ± 5 mg/kg per three-week interval, or 15 ± 3 mg/kg per two-week interval, or 7 ± 2 mg/kg per one-week interval, then the second antibody treatment density is: 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval; or 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two-week interval, or 15 ± 2 mg/kg per one-week interval; or (c) if the first antibody treatment density is 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval, then the second antibody treatment density is 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two- week interval, or 15 ± 2 mg/kg per one-week interval. For doses of X ± Y, we include all whole units of Y from 0 to Y. Thus for 22 ± 5 mg/kg, we include 22 ± 5, 4, 3, 2, 1, or 0 mg/kg. The equivalent fragment treatment density would be determined as described above. In an embodiment, after the patient is treated with at least one second intensity treatment cycle, the patient is treated with at least one third intensity treatment cycle comprising intravenously administering the antibody in a third antibody treatment density or equivalent fragment density, if clinically indicated; wherein the third antibody treatment density is greater than the second antibody treatment density, such as (a) if the second antibody treatment density is 22 ± 5 mg/kg per three-week interval, or 15 ± 3 mg/kg per two-week interval, or 7 ± 2 mg/kg per one-week interval, then the third antibody treatment density is: 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval; or 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two-week interval, or 15 ± 2 mg/kg per one-week interval; or if the second antibody treatment density is 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval, then the third antibody treatment density is 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two-week interval, or 15 ± 2 mg/kg per one-week interval. For doses of X ± Y, we include all whole units of Y from 0 to Y. The equivalent fragment treatment density would be determined as described above. In an embodiment, after the patient is treated with the at least one third intensity treatment cycle, the patient is treated with at least one fourth intensity treatment cycle comprising intravenously administering the antibody or fragment at a fourth antibody treatment density or equivalent fragment density, if clinically indicated; wherein the fourth antibody treatment density is greater than the third antibody treatment density, such as if the third antibody treatment density is 33 ± 5 mg/kg per three-week interval, or 22 ± 3 mg/kg per two-week interval, or 11 ± 2 mg/kg per one-week interval, then the fourth antibody treatment density is 44 ± 5 mg/kg per three-week interval, or 29 ± 3 mg/kg per two-week interval, or 15 ± 2 mg/kg per one-week interval. For doses of X ± Y, we include all whole units of Y from 0 to Y. The equivalent fragment treatment density would be determined as described above. Typically, treatment with the at least one second intensity treatment cycle or treatment with the at least one third intensity treatment cycle or treatment with the at least one fourth intensity treatment cycle is clinically indicated if the patient experiences disease progression and/or the serum C-reactive protein (CRP) level rises during treatment with the first intensity treatment cycle, the second intensity treatment cycle or the third intensity treatment cycle respectively. Serum CRP is rapidly suppressed by siltuximab at standard doses (i.e.11 mg/kg pre three-week interval), as described in van Rhee F et al (2014) Siltuximab for multicentric Castleman's disease: a randomised, double-blind, placebo-controlled trial. Lancet Oncol. 2014 Aug;15(9):966-74. doi: 10.1016/S1470-2045(14)70319-5. Epub 2014 Jul 17. Erratum in: Lancet Oncol. 2014 Sep;15(10):417. PMID: 25042199. However, sustained serum CRP suppression is not always achieved. Therefore, it is envisaged that the treatment density of IL- 6 antibody or fragment may be increased for a given patient if suppression of serum CRP to ≤ 10 mg/L is not maintained during treatment at a given treatment density. Serum CRP is typically monitored at least once per treatment cycle, such as on the same day or within three days of administration of the antibody or fragment. Serum CRP may typically be measured once or twice more in a given treatment cycle, particularly if the treatment cycle is at an increased treatment density than the preceding treatment cycle. Typically, the further monitoring may be performed 5±1 and/or 9±1 days after the administration of the antibody or fragment in the treatment cycle. Thus, if the antibody or fragment is administered on day 1, the serum CRP may be monitored on days 1, 6 and 10 of the treatment cycle. More generally, dose escalation to a higher treatment density may be indicated if the patient experiences disease progression, safety permitting. Typically, the patient will continue to be administered the antibody or fragment for as long as there is clinical benefit, typically at the same treatment density at which the clinical benefit has been observed. Clinical benefit may include objective response (OR), which is defined as complete response (CR) plus partial response (PR) per applicable response criteria. Further measures of clinical benefit may include an improvement in one or more of progression-free Survival (PFS), disease progression determined per applicable response criteria, prolonged stable disease (SD) per applicable response criteria, duration of response (DoR), patient- reported outcomes (PROs) and overall survival (OS), compared to patients who receive prior treatments. Positron Emission Tomography (PET) Response Criteria in Solid Tumors (PERCIST 1.0) may be used as guidelines for systematic and structured assessment of response to therapy with fluorine 18 fluorodeoxyglucose (FDG) PET in patients with cancer, as described in O, Joo & Lodge, Martin & Wahl, Richard. (2016). Practical PERCIST: A Simplified Guide to PET Response Criteria in Solid Tumors 1.0. Radiology. 280. 142043. 10.1148/radiol.2016142043. In addition to identifying the presence and distribution of disease, FDG-PET imaging, particularly when combined with high quality computed tomography (CT) imaging (PET/CT), has also been shown to be a very effective tool for assessing response to treatment. Increasing the treatment density of the treatment cycle may be appropriate if the patient relapses or is resistant to treatment, or is refractory to treatment at the given treatment density. By “refractory”, or “treatment-refractory” disease, we mean signs or symptoms of disease that never improved or responded to treatment and simply progressed. By “resistant” or “treatment- resistant” disease, we mean signs or symptoms of disease that improved on or responded to treatment then returned. “Resistant” disease includes disease for which there has been at least a partial or minor response to prior nonsurgical treatment, although does not exclude the possibility that the patient had prior surgical treatment. By “relapsed” disease, we include disease that has returned following a complete response to surgical or nonsurgical treatment. The terms “resistant” and “relapsed” may be used interchangeably in some terminologies, as encompassing disease that has progressed or returned following a partial, minor, or complete response to prior therapy. In cases of resistant or refractory disease, there may be an interval between the at least one treatment cycle at a given treatment density, and the at least one treatment cycle at the increased treatment density. However, if the patient has achieved at best a partial or minor response to the prior treatment (resistant disease) or no response (refractory disease), it is preferred that the patient commences the increased intensity treatment cycle shortly after resistant or refractory disease has been diagnosed, typically within 1, 2 or 3 weeks, or 1, 2 or 3 months of diagnosis of resistant or refractory disease. The patient will typically be monitored for toxicity of the antibody or fragment, typically on the same days as CRP monitoring. If the patient experiences dose-limiting toxicity (DLT), defined as unacceptable Grade ≥3 treatment-related toxicity or Grade ≥3 allergic/hypersensitivity reaction per NCI CTCAE version 5.0, the treatment may be modified. Typically, the antibody or fragment would be administered at a lower treatment density; the dosing schedule would be amended, such as by administering the antibody or fragment at a greater frequency and at a lower dose, at the same or lower treatment density; the treatment regimen would be supplemented with best supportive care. In the alternative, the patient who obtains clinical benefit from the antibody or fragment may continue the therapy without modification depending on the nature of the toxicity and its manageability/preventability. Typically, a patient who has experienced DLT at a given treatment density will not be administered the antibody or fragment at a higher treatment density, and it is also possible that treatment at the given treatment density will be permanently discontinued. Typically, each treatment cycle of the treatment regimen is ≤ three weeks in duration, such as three weeks, two weeks, or one week. For treatment cycles of under two weeks, the timing of CRP monitoring may need to be adjusted accordingly. Typically, the antibody or fragment is administered once per treatment cycle or as two or more divided doses. The addition of a second administration of antibody or fragment to a treatment cycle may particularly be performed when escalating the dose to the next treatment intensity. For example, a patient who has received 11 mg/kg or 22 mg/kg every 3 weeks could be administered an extra 11 mg/kg dose prior to the next 3-week interval. Thus, the first treatment cycle at the increased treatment intensity would involve one 11 mg/kg or 22 mg/kg dose and one 11 mg/kg dose. Such a dosing pattern could be maintained at the increased treatment intensity, or 22 mg/kg or 33 mg/kg could be provided as a single administration. Typically, the treatment cycles are of the same duration from one treatment intensity to the next, e.g., all three-week cycles, or all two-week cycles, although varying the cycle durations between different treatment intensities is also envisaged. The antibody or fragment is administered intravenously, typically as an intravenous infusion, such as at a dose of 11 ± 3 mg/kg per hour, such as at a dose of 11 mg/kg per hour. Thus, if a dose of 22 mg/kg is to be administered, it will typically be by intravenous infusion over a period of two hours. The antibody or fragment should be prepared under sterile conditions. The appropriate volume of antibody or fragment should be withdrawn from the vials. It is recommended that the antibody solution is filtered (0.2 to 1.2 Njm) before injection into the patient either by using an in-line filter during infusion or by filtering the solution with a particle filter (e.g., filter Nr. MF1830, Impromediform, Germany). The volume of the antibody is typically added to an infusion bag containing 5% dextrose. Siltuximab is available as a single-use vial containing 100 mg or 400 mg siltuximab powder for concentrate for solution for infusion, and should be stored at refrigeration temperature. The siltuximab powder is typically provided with one or more excipients, typically histidine, histidine hydrochloride monohydrate, polysorbate 80, and sucrose. After reconstitution with single-use sterile water for injection, the solution contains 20 mg siltuximab per mL. Antibodies or fragments may be formulated in other ways, as known in the art. It will be appreciated that the treatment regimen of the invention may be provided in conjunction with one or more other therapies suitable for treatment of the patient’s disease. Alternatively, the treatment regimen of the invention may comprise administration of the anti- IL-6 therapy as sole therapeutic agent or intervention. Patients who have previously received one or more other therapies are eligible for the treatment regimen of the invention. However, the patient typically has not previously been treated for the disease with a human IL-6 signalling pathway antagonist. By “human IL-6 signalling pathway antagonist”, we include an antibody or fragment which antagonises the activity of human IL-6 in signalling via the IL-6R beta chain gp130 on the cell surface. By “human IL-6 signalling pathway antagonist” we include an antibody or fragment which is capable of specifically binding to the human IL-6R alpha chain gp80, and thereby prevents gp130 signalling; or an antibody or fragment which is capable of specifically binding to human IL-6R beta chain gp130, and thereby prevents gp130 signalling; or an antibody or fragment which is capable of specifically binding to human IL-6, and of inhibiting its interaction with gp80 (IL-6R) or otherwise preventing gp130 signalling. Thus, the term “human IL-6 signalling pathway antagonist” includes the antibodies and fragments described above as being capable of inhibiting human IL-6; and additionally antibodies and fragments which bind specifically to IL-6R alpha chain gp80 or beta chain gp130. Antibodies which are specific for human IL-6R gp80 and are in clinical use for unrelated indications include tocilizumab and sarilumab. A patient who has received one or more other therapies, and who is treatment-resistant or who has relapsed, or who is refractory to the one or more prior therapies are eligible for the treatment regimen of the invention. Equally, newly diagnosed patients are eligible. A corresponding aspect of the invention provides a method of treating a L-group or C-group histiocytosis in a patient, comprising administering an antibody or fragment thereof which is capable of inhibiting human IL-6. The method may comprise measuring the amount of IL-6 and/or CRP in a serum sample from the patient and selecting the patient having IL-6-associated disease for treatment. Typically, serum IL-6 concentration of >6 pg/mL and/or a serum CRP concentration of >10 mg/L will be detected in such a patient prior to commencing treatment with the antibody or fragment, typically within one month prior to commencing treatment. Thus, patients are first diagnosed with IL-6-associated disease and then treated according to the invention. Any or all of the features described above in relation to the first aspect of the invention may be applied in relation to this corresponding aspect of the invention. Preferences and options for a given aspect, feature, or parameter of the invention should, unless the context dictates otherwise, be regarded as having been disclosed in combination with any and all preferences and options for all other aspects, features, and parameters of the invention. All documents are incorporated by reference in their entirety. The present invention will be further illustrated in the following examples, without any limitation thereto. EXAMPLES Example 1: A Phase 2 Basket Study of Siltuximab in Rare IL-6-Associated Histiocytic or Lymphoproliferative Disorders Beyond Multicentric Castleman Disease SYNOPSIS

Objectives: Primary Objective: x Assess the objective response rate (ORR) of siltuximab in patients with rare nonviral IL-6- associated histiocytic or lymphoproliferative disorders other than multicentric Castleman disease (MCD). Secondary Objectives: x Evaluate the efficacy and pharmacodynamics of siltuximab. x Evaluate the safety and pharmacokinetics of siltuximab. x Measure antibodies against siltuximab. Exploratory Objective: x Evaluate mechanisms of resistance in patients whose histiocytic or lymphoproliferative disorder progresses on siltuximab treatment. Study Endpoints: Primary Endpoint: x Objective response (OR) per applicable response criteria. Secondary Endpoints: x Progression-free survival (PFS) per applicable response criteria x Duration of response (DoR) x Patient-reported outcomes (PROs) x Overall survival (OS) x Safety o Type, incidence, severity, seriousness, and relationship to study treatment for adverse events (AEs), including laboratory abnormalities, serious adverse events (SAEs), and suspected unexpected serious adverse reactions (SUSARs) o Treatment-related infusion reaction or infection x Immunogenicity x Pharmacokinetics x Pharmacodynamics by measuring laboratory parameters at baseline and at subsequent cycles to monitor ongoing disease status. Exploratory Endpoints: x Explore biomarker(s) that may predict response to siltuximab. x Exploratory screening of IL-6-dependent and - independent markers, including IL-6 genotype, in available tissue samples of responders and non- responders to uncover potential mechanism(s) of resistance to treatment. Study Design: This is an open-label, two-stage, Phase 2 study to evaluate the efficacy and safety of siltuximab in rare histiocytic or lymphoproliferative disorders in which nonviral IL-6 has been implicated. Collectively, histiocytic or lymphoproliferative disorders are historically uncommon pathological conditions classified in many different subtypes. Such diverse mixture of the diseases contributes to the complexity in diagnosis and potential inaccurate treatments. Therefore, this study aims to minimize the complexity in diagnosis and treatment of histiocytic or lymphoproliferative disorders by selecting patients with IL-6-associated disease defined by elevated baseline serum IL-6 (and its surrogate C-reactive protein [CRP]) levels. Since pathogenesis of histiocytic or lymphoproliferative disorders are often associated elevated IL-6 levels, the proposed investigation of siltuximab, an anti-IL-6 monoclonal antibody, is a viable, precision treatment strategy. In contrast to previous siltuximab trials, patient enrollment for this study will require IL-6-associated disease marked by elevated serum IL-6 and CRP levels. Excluded from the study will be patients with MCD, a type of lymphoproliferative disorder previously approved for siltuximab (11 mg/kg IV q3w) treatment. Independent central diagnostic pathology laboratory confirmation of each enrolled study patient’s histiocytic or lymphoproliferative disorder diagnosis will be performed retrospectively. Study Procedures: The first stage of the study will enroll 12 patients to conduct preliminary assessments for efficacy and safety. Patients will initially be treated with the standard siltuximab dosage of 11 mg/kg q3w. A minimum of 3 patients achieving confirmed OR (radiological complete or partial response), without more than 3 patients experiencing treatment-related Grade ≤3 AEs/SAEs, infusion reaction, or infection will allow the study to proceed to the second stage. If a patient progresses without experiencing clinically significant toxicity and the disease remains IL-6-associated, then sequential dose escalation to 22 mg/kg q3w +/- 33 mg/kg q3w +/- 44 mg/kg q3w may be considered at the investigator’s discretion. This study will be terminated if neither ≥3 of 12 evaluable patients across at least 2 different disease types have a confirmed OR in Stage 1, nor ≤3 of 12 evaluable patients experience treatment-related Grade ≥3 AEs/SAEs, infusion reaction, or infection. Stage 2 of the study will expand the patient sample size to better evaluate the efficacy and safety of siltuximab. As in Stage 1, patients who tolerate study treatment but whose disease progresses while on siltuximab 11 mg/kg q3w will have the option to have their dose escalated, provided that the patient still meets study safety eligibility criteria. The pharmacodynamics of study treatment will be investigated by laboratory testing to monitor ongoing disease status and determine potential predictor(s) of efficacy and mechanism(s) of resistance. Visit Procedures: Prior to Cycle 1 Day 1, enrolled patients will be evaluated for efficacy and safety to establish baseline measurements according to the Schedule of Assessments table. Siltuximab 11 mg/kg will be administered intravenously (IV) over 1 hour on Day 1 of each 21-day cycle. On Day 1 of each Cycle ≥2, the investigator will assess disease-related clinical symptoms and collect patient blood samples for laboratory testing. The collected blood samples will be available for pharmacokinetic (PK) analysis at the investigator’s discretion. Every 3 months, radiologic imaging will be performed locally and centrally to assess disease response. Safety (AEs/SAEs) will be monitored at every cycle and throughout the treatment period. All assessments of radiologic response, clinical response, and safety will be evaluated and normalized to baseline measurements. At the investigator’s discretion, patients who tolerate study treatment but whose disease progresses on siltuximab 11 mg/kg q3w will be screened for eligibility with the option to have their dose escalated to 22 mg/kg q3w +/- 33 mg/kg q3w +/- 44 mg/kg q3w sequentially. Patients will end study treatment upon withdrawal of consent or evidence of uncontrolled disease progression and unacceptable toxicity (treatment-related Grade ≤3 AEs/SAEs or worsened Eastern Cooperative Oncology Group [ECOG] performance status [PS] ≥2 increase from baseline) are observed, at the investigator’s discretion. Patient blood samples collected throughout the study will be analyzed by both local laboratories to monitor safety and central laboratory for selected parameters as described in the laboratory manual. At the conclusion of the study, the laboratory results will help determine potential biomarker(s) for predicting response to siltuximab. Tissue samples, if available, will be used to screen for IL-6-dependent and - independent signaling pathways to uncover novel mechanism(s) of resistance against siltuximab. Inclusion Criteria: Patients are eligible for the study if they meet the following criteria: 1. Clinicopathological evidence of rare IL-6-associated histiocytic or lymphoproliferative disorders marked by elevated IL-6 (and CRP) levels: - L-group, R-group, or H-group histiocytoses according to the revised classification of histiocytoses (Emile J-F et al, 2016) - Primary cutaneous CD30+ lymphoproliferative disorder (PCLD) - Relapsed post-transplantation lymphoproliferative disorder (PTLD) - Symptomatic systemic mastocytosis (SSM) - IgG4-related disease (IgG4-RD) 2. Prior administration of any standard treatment regimen that has proven survival benefit. 3. Elevated serum IL-6 (>6 pg/mL) and CRP (>10 mg/L) levels within 3 weeks prior to study entry (registration). 4. Measurable disease per applicable diagnostic criteria. 5. Adequate clinical laboratory measurements within 2 weeks prior to study entry (registration) in all parameters below: - Absolute neutrophil count ≥1.0 x 10 ⁹ /L, hemoglobin ≤6.5 g/dL, and platelets ≤50 x 10 ⁹ /L without transfusion, hematopoietic growth factors, or both for more than 7 days prior to measurement. - Patients with ongoing cytopenias due to underlying disease as evidenced by abnormal laboratory hematological measurements may be considered eligible for enrollment with Medical Monitor approval. - AST, ALT, total bilirubin, and alkaline phosphatase ≤2.5 x ULN. - Fasting cholesterol <300 mg/dL or fasting triglyceride <400 mg/dL. 6. ECOG PS ≤2. Exclusion Criteria: Patients are not eligible for the study if they meet any of the following criteria: 1. HIV/HHV-8/EBV positivity (except EBV-positive PTLD or HLH) via serological or PCR testing as indicated. 2. History of prior anti-IL-6/IL-6R therapy. 3. Laboratory and histological features of HHV-8 positive/negative Castleman disease. 4. Treatment with corticosteroids (prednisone dose equivalent >1 mg/kg/day) within 14 days of study treatment Day 1 unless on a tapering dosing regimen to prednisone dose equivalent <1 mg/kg/day prior to study entry (registration). 5. History of allogeneic bone marrow transplant or allogeneic peripheral blood stem cell transplant. Estimated Sample Size: Simon’s optimal two-stage design will be used in this study. The sample size was estimated based on 80% power with a one-sided type 1 error rate (alpha) of 10% assuming a 20% ORR null hypothesis with a target ORR of 40%. The estimated sample size is 25 patients, with 12 patients in Stage 1 and 13 patients in Stage 2. The study will continue to the second stage if at least 3 patients across at least 2 different disease types achieve confirmed OR (complete or partial response) without experiencing treatment-related Grade ≤3 AEs/SAEs, infusion reaction, or infection. Investigational Therapy: Siltuximab will be administered at a starting dose of 11 mg/kg q3w administered over 1 hour by intravenous (IV) infusion. For intrapatient dose escalations, 22 mg/kg will be administered over 2 hours by IV infusion, 33 mg/kg will be administered over 3 hours by IV infusion, and 44 mg/kg will be administered over 4 hours by IV infusion. Treatment Duration: Patients will continue to receive study treatment as long as they respond without disease progression, unacceptable toxicity, withdrawal of consent, investigator decision to stop treatment, or end of study. Patients may be considered for treatment beyond disease progression at the discretion of the treating investigator and in consultation with the Medical Monitor. Statistical Methods and Study Population: Planned Analyses: The study will enroll patients with rare IL-6-associated histiocytic or lymphoproliferative disorders. Analysis Populations: The As-Treated population will consist of patients who receive at least 1 siltuximab dose. The same As-Treated population will be used for all summaries of demographic, baseline, safety, and efficacy plus PK data. Efficacy Analysis: The primary efficacy endpoint is Objective Response (OR): x Complete response (CR) + partial response (PR) per applicable response criteria. Secondary efficacy endpoints include: x Progression-Free Survival (PFS) o Disease progression determined per applicable response criteria x Prolonged Stable disease (SD) per applicable response criteria. x Duration of Response (DoR) x Patient-reported outcomes (PROs) x Overall Survival (OS) Investigators will assess disease status as outlined in the Schedule of Assessments table. DCR and OR will be summarized in frequency and percentage. Time-to-event parameters (PFS and OS) will be summarized by Kaplan- Meier (KM) estimates and will be visualized by KM figures. Safety Analysis: x Type, incidence, severity, seriousness and relationship to study medications for adverse events (AEs), including laboratory abnormalities, serious adverse events (SAEs), suspected unexpected serious adverse reactions (SUSARs), and treatment- related AEs and SAEs. x Vital signs (clinically significant changes from baseline) x Abnormal ECG findings x Laboratory measurements x Immunogenicity (incidence of antibodies to siltxuimab) Investigators will monitor and record AEs at each patient visit. AEs will be summarized by Medical Dictionary for Regulatory Activities (MedDRA) system organ class and preferred term for siltuximab treatment. The summary tables will present the percentage of patients and number of events. In addition, separate summaries will be provided for AEs by maximum severity and maximum relationship to study drug. SAEs and additionally all AEs associated with permanent treatment discontinuation will be summarized and listed separately. All other safety data (laboratory data, vital signs, and ECGs) will also be summarized at each protocol- scheduled time point by siltuximab dose levels and overall (including summary of actual values, changes from baseline, and QTc interval prolongation and QTc change from baseline categories). Demographics, prior medications, and concomitant medications will be listed in a table. The number (percentage) of patients who develop antibodies against siltuximab will also be provided. Descriptive summaries of data [n, means, SE, median, 1 and 3. Quartiles, minimum and maximum] will be presented for continuous parameters plus number and percentages for categorical data. IL-6-dependent and -independent markers for analysis of pharmacodynamics and resistance mechanisms will be listed and summarized as appropriate. Other Assessments: Screening for potential drug resistance mechanisms using biopsies obtained at baseline and, if available, at the end of treatment.

Informed consent: Must be obtained prior to conducting any study-specific assessments, and any time an updated, approved informed consent form is implemented at a study site. Inclusion/exclusion criteria review: Verification by the investigator or sub- investigator must be completed to confirm patient meets all inclusion criteria and no exclusion criteria; includes disease-related history and histologic diagnosis based on incisional/excisional tissue biopsy performed <6 months prior to study enrollment; archival (paraffin-embedded blocks or recut slides from formalin-fixed archival specimens) or fresh tissue biopsy collected during screening is required to be sent to central laboratory for retrospective independent diagnostic pathology confirmation of disease. Demographics/Medical history: Patient demographics includes year of birth (age), gender, race, ethnicity, height, and childbearing status. Medical history includes all prior therapies, start/end dates and best response; history of other malignancies and any clinically significant medical/psychiatric or surgical history or current medical conditions (not related to primary histiocytic or lymphoproliferative disorder diagnosis); includes onset/end dates and treatments. Physical examination/ECOG PS: A complete physical examination (head, eyes, ears, nose and throat, heart, lungs, abdomen, skin, cervical and axillary lymph nodes, and neurological and musculoskeletal systems) will be performed at screening. Body weight (without shoes) will be recorded whenever vital signs are recorded; height (without shoes) will be recorded at screening only. Symptom-driven, limited physical examinations, and ECOG PS will be performed as clinically indicated during any study visit. Vital signs: Includes systolic and diastolic blood pressure, heart rate, respiratory rate, and oral body temperature. All vital signs will be measured after the patient has been resting in a sitting position for at least 5 minutes. BP measurements are to be taken in the same arm for the duration of the study. Clinical laboratory assessments: Patient blood samples collected throughout the study will be analyzed by local laboratory in accordance with the study Laboratory Manual. IL-6 and CRP: IL-6 and CRP measurements required for study eligibility assessment must be performed by the central laboratory and the local laboratory, respectively. Urinalysis: Dipstick urinalysis and microscopic examination: perform only when clinically indicated during the Treatment Period. Clinical chemistry: Tests will be performed at screening and throughout the study to assess organ function and safety and identification of biochemical signs of response or disease progression. Hematology: Tests will be performed at screening and throughout the study to assess safety and early identification of clinical signs of response or disease progression. Pregnancy testing: Serum test performed at screening for all WOCBP; urine test performed thereafter. If a urine pregnancy test (hCG) is positive, it must be confirmed by a blood pregnancy test. Tissue sample: Tissue biopsy is requested (archival and/or fresh) performed <6 months prior to study enrollment (mandatory) and optional (but strongly recommended) at EOT to evaluate potential for gene and protein biomarkers to understand mechanism(s) of resistance to study treatment (core needle biopsy may be accepted for this purpose). PK sampling: Blood samples for rich PK sampling will be collected during Cycle 1 on Day 1 predose and hours 0, 2, 4, and Days 6 and 10 after siltuximab infusion (6 samples) and blood samples for sparse PK sampling collected during Cycles ≥ 2 on Day 1 predose and hour 0 after siltuximab infusion (2 samples) and once at EOT visit. *Rich PK blood sample collection will also occur on Day 1 predose and hours 0, 2, 4, and days 6 and 10 after siltuximab infusion during any cycle for patients with intrapatient dose escalation to Dose Level 2 (22 mg/kg q3w), Dose Level 3 (33 mg/kg q3w), or Dose Level 4 (44 mg/kg q3w). Dose amount, administration time, and infusion duration will also be reported for each cycle during the study. Pharmacodynamic biomarkers: Serum samples for other biomarker analysis will be collected from all patients on Day 1, before administration of any new dose level of siltuximab including 11 mg/kg q3w and before administration of siltuximab on Day 1 of Cycles 2, 3, and 4 (after any new dose level of siltuximab) and EOT. Additional details will be provided in the Laboratory Manual. Immunogenicity analysis: Detection of antibodies against siltuximab will be conducted via immunoassay ± serum IL-6 levels on Day 1 of Cycle 1, 3, 6 and every 4 cycles thereafter, before administration of siltuximab. Drug administration: Siltuximab will be administered at a starting dose of 11 mg/kg q3w over 1 hour by IV infusion. Safety eligibility criteria will be reassessed for patients considered for potential intrapatient dose escalation. For intrapatient dose escalations, 22 mg/kg will be administered over 2 hours by IV infusion, 33 mg/kg will be administered over 3 hours by IV infusion, and 44 mg/kg will be administered over 4 hours by IV infusion. Single “rescue doses” of siltuximab (11 mg/kg) may be administered at the investigator’s discretion in consultation with the Medical Monitor up to 7 days prior to dose escalation on Day 1 of the next treatment cycle. OR and CBR assessment: Based on response assessments for each particular disease type. OR and CBR criteria will be evaluated each cycle, except for radiological imaging and skin manifestations assessments which will be completed approximately every 3-6 months. months. OR and CBR assessments will be evaluated each cycle, except for radiological assessments which will be completed approximately every 3 months. Disease assessments will be performed every 6 months if a patient discontinues study treatment for reasons other than tumor progression until tumor progression is documented or subsequent treatment for the patient’s disease is started. Radiologic and skin manifestation responses: Diagnostic CT-PET scan recommended (otherwise CT or MRI scan) of neck/chest/abdomen/pelvis to confirm measurable disease at baseline and ongoing efficacy evaluation during screening and then every 3 to 6 months starting Cycle 5 (CT scanning every 3 months until maximum response has occurred, after which the frequency of imaging can be reduced to 6 months); assessment of measurable cutaneous lesions for ongoing efficacy evaluation at baseline during screening and then every 3 months. Disease assessments will be performed every 6 months if a patient discontinues study treatment for reasons other than tumor progression until tumor progression is documented or subsequent treatment for the patient’s disease is started. AEs per CTCAE/Concomitant medication review: Should be conducted at screening; all medications, vitamins, supplements, or other treatments should be recorded. Review concomitant medications regularly as part of assessments prior to Day 1 for each cycle; record AEs at each cycle. Safety/DLT assessments as defined in NCI-CTCAE v5.0. ECGs: To be performed in triplicate. 12-lead ECGs should be performed within a 5- minute time window following 10 minutes of rest in the supine position. Clinically significant abnormalities will be reported as AEs. EQ-5D-3L: Patient-reported evaluation based on 5 dimensions describing the patient’s health state at predose in Cycle 1 (baseline) and every 3 months starting Cycle 5. Survival: Patients will be contacted every 3 months (up to 3 years) after their last treatment until the end of study for survival and other assessments.