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      Clinical use of biologics in vasculitis syndromes

      review-article
      Biologics : Targets & Therapy
      Dove Medical Press
      anti-TNF-alpha, rituximab, tocilizumab, vasculitides

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          Abstract

          Vasculitis syndromes are relative rare conditions but can cause significant mortality and morbidity if not treated adequately. Recent advances in immunosuppressant therapy have radically changed the course of these diseases. However, the standard therapy is not always well tolerated by patients, and some cases are refractory to treatment. New therapeutic possibilities have emerged with the use of so-called “biologics,” a new class of genetically engineered drugs used for inflammatory rheumatic diseases, including rheumatoid arthritis, ankylosing spondylitis, and psoriatic arthritis. In the present review, summarized are the most recent data on the efficacy and safety of biologics in the treatment of vasculitis syndromes that cannot be treated with standard therapy.

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          Most cited references62

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          IL-6 mediates hypoferremia of inflammation by inducing the synthesis of the iron regulatory hormone hepcidin.

          Hypoferremia is a common response to systemic infections or generalized inflammatory disorders. In mouse models, the development of hypoferremia during inflammation requires hepcidin, an iron regulatory peptide hormone produced in the liver, but the inflammatory signals that regulate hepcidin are largely unknown. Our studies in human liver cell cultures, mice, and human volunteers indicate that IL-6 is the necessary and sufficient cytokine for the induction of hepcidin during inflammation and that the IL-6-hepcidin axis is responsible for the hypoferremia of inflammation.
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            Complementary DNA for a novel human interleukin (BSF-2) that induces B lymphocytes to produce immunoglobulin.

            When stimulated with antigen, B cells are influenced by T cells to proliferate and differentiate into antibody-forming cells. Since it was reported that soluble factors could replace certain functions of helper T cells in the antibody response, several different kinds of lymphokines and monokines have been reported in B-cell growth and differentiation. Among these, human B-cell differentiation factor (BCDF or BSF-2) has been shown to induce the final maturation of B cells into immunoglobulin-secreting cells. BSF-2 was purified to homogeneity and its partial NH2-terminal amino-acid sequence was determined. These studies indicated that BSF-2 is functionally and structurally unlike other known proteins. Here, we report the molecular cloning, structural analysis and functional expression of the cDNA encoding human BSF-2. The primary sequence of BSF-2 deduced from the cDNA reveals that BSF-2 is a novel interleukin consisting of 184 amino acids.
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              The Innate Mononuclear Phagocyte Network Depletes B Lymphocytes through Fc Receptor–dependent Mechanisms during Anti-CD20 Antibody Immunotherapy

              Anti-CD20 antibody immunotherapy effectively treats non-Hodgkin's lymphoma and autoimmune disease. However, the cellular and molecular pathways for B cell depletion remain undefined because human mechanistic studies are limited. Proposed mechanisms include antibody-, effector cell–, and complement-dependent cytotoxicity, the disruption of CD20 signaling pathways, and the induction of apoptosis. To identify the mechanisms for B cell depletion in vivo, a new mouse model for anti-CD20 immunotherapy was developed using a panel of twelve mouse anti–mouse CD20 monoclonal antibodies representing all four immunoglobulin G isotypes. Anti-CD20 antibodies rapidly depleted the vast majority of circulating and tissue B cells in an isotype-restricted manner that was completely dependent on effector cell Fc receptor expression. B cell depletion used both FcγRI- and FcγRIII-dependent pathways, whereas B cells were not eliminated in FcR common γ chain–deficient mice. Monocytes were the dominant effector cells for B cell depletion, with no demonstrable role for T or natural killer cells. Although most anti-CD20 antibodies activated complement in vitro, B cell depletion was completely effective in mice with genetic deficiencies in C3, C4, or C1q complement components. That the innate monocyte network depletes B cells through FcγR-dependent pathways during anti-CD20 immunotherapy has important clinical implications for anti-CD20 and other antibody-based therapies.
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                Author and article information

                Journal
                Biologics
                Biologics
                Biologics: Targets & Therapy
                Biologics : Targets & Therapy
                Dove Medical Press
                1177-5475
                1177-5491
                2012
                2012
                25 October 2012
                : 6
                : 371-378
                Affiliations
                Division of Clinical Immunology and Rheumatology, Department of Biotechnology and Medical-Surgical Sciences, Sapienza University of Rome, Italy
                Author notes
                Correspondence: Marino Paroli, Sapienza University of Rome, Piazzale, Aldo Moro 5, 00161 Roma, Italy, Tel +39 0773 47 6814, Fax +39 0773 47 6813, Email marino.paroli@ 123456uniroma1.it
                Article
                btt-6-371
                10.2147/BTT.S37537
                3484501
                23118526
                a262c638-8fe0-4bba-80c2-ce255e6ec4d0
                © 2012 Paroli, publisher and licensee Dove Medical Press Ltd.

                This is an Open Access article which permits unrestricted noncommercial use, provided the original work is properly cited.

                History
                : 24 October 2012
                Categories
                Review

                Molecular medicine
                anti-tnf-alpha,rituximab,tocilizumab,vasculitides
                Molecular medicine
                anti-tnf-alpha, rituximab, tocilizumab, vasculitides

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