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      Mechanisms of tissue injury in lupus nephritis

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      Author(s): 1 , 2 , 1 , 2 ,
      Publication date (Electronic):
      Journal: Arthritis Research & Therapy
      Publisher: BioMed Central

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          Abstract

          Systemic lupus erythematosus is a prototypic autoimmune disease characterized by autoantibody production and immune complex formation/deposition in target organs such as the kidney. Resultant local inflammation then leads to organ damage. Nephritis, a major cause of morbidity and mortality in patients with lupus, occurs in approximately 50% of lupus patients. In the present review, we provide an overview of the current research and knowledge concerning mechanisms of renal injury in both lupus-prone mouse models and human lupus patients.

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          A Novel Mouse with B Cells but Lacking Serum Antibody Reveals an Antibody-independent Role for B Cells in Murine Lupus

          Owen Chan, Lynn Hannum, Ann Haberman … (1999)
          The precise role of B cells in systemic autoimmunity is incompletely understood. Although B cells are necessary for expression of disease (Chan, O., and M.J. Shlomchik. 1998. J. Immunol. 160:51–59, and Shlomchik, M.J., M.P. Madaio, D. Ni, M. Trounstine, and D. Huszar. 1994. J. Exp. Med. 180:1295–1306), it is unclear whether autoantibody production, antigen presentation, and/or other B cell functions are required for the complete pathologic phenotype. To address this issue, two experimental approaches were used. In the first, the individual contributions of circulating antibodies and B cells were analyzed using MRL/MpJ-Faslpr (MRL/lpr) mice that expressed a mutant transgene encoding surface immunoglobulin (Ig), but which did not permit the secretion of circulating Ig. These mice developed nephritis, characterized by cellular infiltration within the kidney, indicating that B cells themselves, without soluble autoantibody production, exert a pathogenic role. The results indicate that, independent of serum autoantibody, functional B cells expressing surface Ig are essential for disease expression, either by serving as antigen-presenting cells for antigen-specific, autoreactive T cells, or by contributing directly to local inflammation.
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            Expanded double negative T cells in patients with systemic lupus erythematosus produce IL-17 and infiltrate the kidneys.

            Isaac Stillman, A Kolk, Yuang-Taung Juang … (2008)
            Double negative (DN) T cells are expanded in patients with systemic lupus erythematosus (SLE) and stimulate autoantibody production as efficiently as CD4(+) T cells. In this study, we demonstrate that DN T cells from patients with SLE produce significant amounts of IL-17 and IFN-gamma, and expand when stimulated in vitro with an anti-CD3 Ab in the presence of accessory cells. Furthermore, IL-17(+) and DN T cells are found in kidney biopsies of patients with lupus nephritis. Our findings establish that DN T cells produce the inflammatory cytokines IL-17 and IFN-gamma, and suggest that they contribute to the pathogenesis of kidney damage in patients with SLE.
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              Complement deficiencies and systemic lupus erythematosus.

              Anders A. Bengtsson, Lennart Truedsson, Gunnar Sturfelt (2007)
              The complement system involves both the innate and the adaptive immune systems and has important roles in the pathogenesis of SLE. Complement deficiencies within the classical pathway (C1q, C4 and C2) of activation predispose for development of the autoimmune disease SLE. The association between complement deficiencies and SLE could be explained by several mechanisms, including impaired clearance of immune complexes and impaired handling of apoptotic cells, aberrant tolerance induction or changes in cytokine regulation. Also during SLE disease flares, the complement system is activated giving rise to partial deficiency or dysfunction due to consumption. On the other hand, complement also takes part in the inflammatory reaction in the disease that gives rise to the tissue and organ damage. In this review various aspects of the relation between complement and SLE are discussed.
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                Author and article information

                Journal
                Journal ID (nlm-ta): Arthritis Res Ther
                Journal ID (iso-abbrev): Arthritis Res. Ther
                Title: Arthritis Research & Therapy
                Publisher: BioMed Central
                ISSN (Print): 1478-6354
                ISSN (Electronic): 1478-6362
                Publication date (Print): 2011
                Publication date (Electronic): 21 December 2011
                Publication date PMC-release: 21 June 2012
                Volume: 13
                Issue: 6
                Page: 250
                Affiliations
                [1 ]Department of Medicine, Division of Rheumatology, Medical University of South Carolina, 96 Jonathan Lucas St, CSB 912 MSC 637 Charleston, SC 29425-6370, USA
                [2 ]Medical Research Service, Ralph H. Johnson Veterans Affairs Medical Center, 109 Bee Street, Charleston, SC 29401, USA
                Article
                Publisher ID: ar3528
                DOI: 10.1186/ar3528
                PMC ID: 3334648
                PubMed ID: 22192660
                SO-VID: 35aa07ed-4ff9-442f-8cbc-4fc28002de1c
                Copyright © Copyright ©2011 BioMed Central Ltd
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                Subject: Review

                ScienceOpen disciplines: Orthopedics
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                ScienceOpen disciplines: Orthopedics

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