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 CD30+ lymphoproliferative disorders of the skin; and compositions for use in such methods. BACKGROUND TO THE INVENTION CD30+ lymphoproliferative disorders of the skin are characterised by abnormal proliferation of lymphoid cells which typically express CD30, a cell surface cytokine receptor present on activated T- and B-cells. Primary cutaneous CD30+ lymphoproliferative disorders (LPD) comprise a spectrum of conditions with similar histologic and molecular features, but different clinical presentations. According to the World Health Organization (WHO) and European Organization for Research and Treatment (EORTC) classification, this group accounts for 20% of all cutaneous lymphomas (Willemze R, Jaffe ES, Burg G, et al. WHO-EORTC classification for cutaneous lymphomas. Blood. 2005 May 15;105(10):3768–85). Primary cutaneous CD30+ lymphoproliferative disorders encompass lymphomatoid papulosis (LyP), primary cutaneous anaplastic large cell lymphoma (pcALCL) and indeterminate cases. A related condition, secondary cutaneous anaplastic large cell lymphoma (scALCL) is systemic ALCL with skin involvement, where the skin is the most common extra-nodal site. Diagnosis and treatment of CD30+ lymphoproliferative disorders of the skin is described in Sauder MB, O'Malley JT, LeBoeuf NR. CD30+ Lymphoproliferative Disorders of the Skin. Hematol Oncol Clin North Am. 2017;31(2):317-334. doi:10.1016/j.hoc.2016.11.006. LyP is benign, limited to the skin and self-resolves with a 5-year survival rate of 100%, but it is associated with increased risk of secondary malignancy. Management of LyP depends on clinical severity and symptoms. Indications to treat include cases that are diffuse or progressive, are physically symptomatic or lead to disfigurement from significant scarring or pigmentary change. With limited disease burden, active non-treatment may be appropriate and considered first-line. The majority of LyP patients with few lesions are managed with potent topical steroids at the first sign of a new papule; those with more diffuse disease respond to low dose methotrexate or phototherapy. pcALCL is usually limited to the skin and responsive to directed therapies, with a 5-year survival of over 95%. Typical current treatment for pcALCL includes radiotherapy, surgical excision, or low-dose (less than 25 mg/week) methotrexate. Prognosis of sALCL, including scALCL, is related to the expression of the ALK protein. sALCL patients with ALK positive disease have a 5-year survival of 70% while ALK negative disease has a 49% 5-year survival. Extra-nodal involvement of sALCL, such as cutaneous involvement, is a poor prognostic sign. sALCL may be treated by chemotherapy. The antibody-drug conjugate brentuximab vedotin, which binds to CD30, is FDA-approved for treatment of patients with sALCL after failure of at least one prior multi-agent chemotherapy regimen. Crizotinib, a tyrosine kinase inhibitor, is FDA-approved for the treatment of pediatric patients 1 year of age and older and young adults with relapsed or refractory, systemic anaplastic large cell lymphoma (ALCL) that is anaplastic lymphoma kinase (ALK)-positive. 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 reported that serum IL-6 is highly elevated in patients having peripheral T-cell lymphoma (PTCL) (Raziuddin et al (1994) Cancer 73:2426-31). It is suggested that the elevated IL-6 and also TNFĮ may contribute to pathology in PTCL. ALCL, especially ALK-negative ALCL, can be considered a PTCL, unspecified, according to L. Jeffrey Medeiros, MD, Kojo S.J. Elenitoba-Johnson, MD, Anaplastic Large Cell Lymphoma, American Journal of Clinical Pathology, Volume 127, Issue 5, May 2007, Pages 707–722. Furthermore, Horwitz SM et al Blood (2019) 134 (Supplement_1): 466 report positive results of the dual Syk/Jak inhibitor cedulatinib in relapsed/refractory PTCL in a phase II clinical trial. 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 CD30+ lymphoproliferative disorders of the skin. 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 a CD30+ lymphoproliferative disorder of the skin in a patient. A corresponding aspect of the invention provides a method of treating a CD30+ lymphoproliferative disorder of the skin 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 CD30+ lymphoproliferative disorder of the skin 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. CD30+ lymphoproliferative disorders of the skin are classified according to the World Health Organization (WHO) and European Organization for Research and Treatment of Cancer (EORTC) (WHO-EORTC) classification for cutaneous lymphomas, as described in Willemze R, et al. WHO- EORTC classification for cutaneous lymphomas. Blood. 2005 May 15;105(10):3768-85. doi: 10.1182/blood-2004-09-3502. Further information on classification and diagnosis, including the identification of new subsets of lymphomatoid papulosis, and exclusion criteria for diseases which can mimic CD30+ lymphoproliferative disorders of the skin, are described in Sauder MB, O'Malley JT, LeBoeuf NR. CD30+ Lymphoproliferative Disorders of the Skin. Hematol Oncol Clin North Am. 2017;31(2):317-334. doi:10.1016/j.hoc.2016.11.006. Diagnosis is typically based on clinical features, and histopathology and immunohistochemistry analyses of biopsied skin. According to the WHO-EORTC classification, primary cutaneous anaplastic large cell lymphoma (pcALCL) is defined as composed of large cells with an anaplastic, pleomorphic, or immunoblastic cytomorphology and expression of the CD30 antigen by the majority (more than 75%) of tumor cells. pcALCL affects mainly adults with a male to female ratio of 2-3:1. Most patients present with solitary or localized nodules or tumors, and sometimes papules, and often show ulceration. Multifocal lesions are seen in about 20% of the patients. The skin lesions may show partial or complete spontaneous regression, as in LyP. These lymphomas frequently relapse in the skin. Extracutaneous dissemination occurs in approximately 10% of the patients, and mainly involves the regional lymph nodes. Histopathology is characterised by a diffuse, nonepidermotropic infiltrate with cohesive sheets of large CD30 ⁺ tumor cells. Reactive lymphocytes are often present at the periphery of the lesions. Ulcerating lesions may show a LyP-like histology with an abundant inflammatory infiltrate of reactive T cells, histiocytes, eosinophils and/or neutrophils, and relatively few CD30 ⁺ cells. In such cases epidermal hyperplasia may be prominent. The neoplastic cells generally show an activated CD4 ⁺ T-cell immunophenotype with variable loss of CD2, CD5, and/or CD3, and frequent expression of cytotoxic proteins (granzyme B, TIA-1, perforin). Some cases (less than 5%) have a CD8 ⁺ T- cell phenotype. CD30 must be expressed by the majority (more than 75%) of the neoplastic T cells. According to the WHO-EORTC classification, lymphomatoid papulosis (LyP) is defined as a chronic, recurrent, self-healing papulonecrotic or papulonodular skin disease with histologic features suggestive of a (CD30 ⁺ ) malignant lymphoma. LyP generally occurs in adults (median age, 45 years; male-to-female ratio, 1.5:1), but may occur in children as well. LyP is characterized by the presence of papular, papulonecrotic, and/or nodular skin lesions at different stages of development, predominantly on the trunk and limbs. Individual skin lesions disappear within 3 to 12 weeks, and may leave behind superficial scars. The duration of the disease may vary from several months to more than 40 years. In up to 20% of patients LyP may be preceded by, associated with, or followed by another type of malignant (cutaneous) lymphoma, generally MF, a pcALCL, or Hodgkin lymphoma. The histologic picture of LyP is extremely variable. There are currently 5 generally accepted histologic subtypes of LyP (A-E), as well as a recently proposed 6th subtype (F). CD30+ T-cell lymphocytes are the hallmark of all histologic types of LyP, although type B has variable positivity, reported to range from 0 to 77% of the infiltrate. For the avoidance of doubt, we note that CD30- LyP is still regarded as belonging within the family of CD30+ lymphoproliferative disorders of the skin. The majority of LyP cases are CD4+ and CD45RO+; however, type D, type E and LyP in children are CD4í CD8+.29 CD45RO helps to differentiate LyP type D from aggressive epidermotropic CD8+ CTCL with the former being CD45RO+ and the latter being CD45RO-. Further information on the subtypes of LyP is found in Sauder et al, 2017, supra. According to Sauder et al, 2017, supra, pcALCL and LyP can be thought of as a clinical spectrum where indeterminate cases may have clinical and histological features of either, as shown in Table 1. LyP is a benign disorder characterized by recurrent crops of several to hundreds of papulonodules, red or violaceous in colour and measuring up to 20mm, usually on the trunk and extremities. pcALCL is characterized by solitary or grouped red to violaceous nodules or tumors greater than 20mm and may occur anywhere on the body. Indeterminate cases tend to eventually develop clinical features of either LyP or pcALCL over time, and can be distinguished on that basis. Table 1: Clinical features of LyP and pcALCL Anaplastic large cell lymphoma (ALCL) is a rare and heterogeneous malignant tumor, with high expression of CD30 and large cell proliferation, and is classified according to the WHO classification of lymphoid neoplasms. A 2;5 chromosomal translocation has been found in ALCL, and this rearrangement can fuse the amino terminus of nucleophosmin (NPM) nucleolar phosphoprotein gene on chromosome 5q35 to a protein tyrosine kinase gene ALK on chromosome 2p23. ALCL is classified into ALK+ ALCL and ALK- ALCL, according to the expression state of ALK protein, as recognised in the 2016 WHO classification (Swerdlow SH, et al, The 2016 revision of the World Health Organization classification of lymphoid neoplasms. Blood. 2016 May 19;127(20):2375-90). Systemic ALCL commonly presents with B symptoms (fevers, chills, fatigue, night sweats or weight loss) and approximately 20% of cases of sALCL will develop skin lesions. Secondary cutaneous anaplastic large cell lymphoma (scALCL) is systemic ALCL with skin involvement, where the skin is the most common extra-nodal site. Diagnostic criteria are described in Sauder et al, 2017, supra. The lesions tend to be multifocal or generalized in contrast to pcALCL. Cutaneous lymphocyte antigen (CLA) is generally negative in scALCL whereas epithelial membrane antigen (EMA) is positive in scALCL. In scALCL ALK is positive in 50% of cases. Patients for whom the treatment regimen of the invention is intended may have primary cutaneous anaplastic large cell lymphoma, secondary cutaneous anaplastic large cell lymphoma or lymphomatoid papulosis. 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 IgG4lj 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. Response to treatment of cutaneous lymphomas may be assessed according to modified Severity Weighted Assessment Tool (mSWAT) scoring, as described in Kempf, Werner & Mitteldorf, Christina. (2015). Pathologic Diagnosis of Cutaneous Lymphomas. Dermatologic Clinics. 33. 10.1016/j.det.2015.05.002. 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 CD30+ lymphoproliferative disorder of the skin 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

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.

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