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      A novel anti-inflammatory role for secretory phospholipase A 2 in immune complex-mediated arthritis

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          Abstract

          Phospholipase A 2 (PLA 2) catalyses the release of arachidonic acid for generation of lipid mediators of inflammation and is crucial in diverse inflammatory processes. The functions of the secretory PLA 2 enzymes (sPLA 2), numbering nine members in humans, are poorly understood, though they have been shown to participate in lipid mediator generation and the associated inflammation. To further understand the roles of sPLA 2 in disease, we quantified the expression of these enzymes in the synovial fluid in rheumatoid arthritis and used gene-deleted mice to examine their contribution in a mouse model of autoimmune erosive inflammatory arthritis. Contrary to expectation, we find that the group V sPLA 2 isoform plays a novel anti-inflammatory role that opposes the pro-inflammatory activity of group IIA sPLA 2. Mechanistically, group V sPLA 2 counter-regulation includes promotion of immune complex clearance by regulating cysteinyl leukotriene synthesis. These observations identify a novel anti-inflammatory function for a PLA 2 and identify group V sPLA 2 as a potential biotherapeutic for treatment of immune-complex-mediated inflammation.

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          The American Rheumatism Association 1987 revised criteria for the classification of rheumatoid arthritis.

          D McShane, D. Bloch, Emma Healey … (1988)
          The revised criteria for the classification of rheumatoid arthritis (RA) were formulated from a computerized analysis of 262 contemporary, consecutively studied patients with RA and 262 control subjects with rheumatic diseases other than RA (non-RA). The new criteria are as follows: 1) morning stiffness in and around joints lasting at least 1 hour before maximal improvement; 2) soft tissue swelling (arthritis) of 3 or more joint areas observed by a physician; 3) swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints; 4) symmetric swelling (arthritis); 5) rheumatoid nodules; 6) the presence of rheumatoid factor; and 7) radiographic erosions and/or periarticular osteopenia in hand and/or wrist joints. Criteria 1 through 4 must have been present for at least 6 weeks. Rheumatoid arthritis is defined by the presence of 4 or more criteria, and no further qualifications (classic, definite, or probable) or list of exclusions are required. In addition, a "classification tree" schema is presented which performs equally as well as the traditional (4 of 7) format. The new criteria demonstrated 91-94% sensitivity and 89% specificity for RA when compared with non-RA rheumatic disease control subjects.
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            Organ-specific disease provoked by systemic autoimmunity.

            Valerie Kouskoff, Anne-Sophie Korganow, Veronique Duchatelle … (1996)
            Rheumatoid arthritis (RA) is a chronic joint disease characterized by leukocyte invasion and synoviocyte activation followed by cartilage and bone destruction. Its etiology and pathogenesis are poorly understood. We describe a spontaneous mouse model of this syndrome, generated fortuitously by crossing a T cell receptor (TCR) transgenic line with the NOD strain. All offspring develop a joint disease highly reminiscent of RA in man. The trigger for the murine disorder is chance recognition of a NOD-derived major histocompatibility complex (MHC) class II molecule by the transgenic TCR; progression to arthritis involves CD4+ T, B, and probably myeloid cells. Thus, a joint-specific disease need not arise from response to a joint-specific antigen but can be precipitated by a breakdown in general mechanisms of self-tolerance resulting in systemic self-reactivity. We suggest that human RA develops by an analogous mechanism.
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              From systemic T cell self-reactivity to organ-specific autoimmune disease via immunoglobulins.

              Anne-Sophie Korganow, Hong Ji, Sara Mangialaio … (1999)
              Rheumatoid arthritis is a common and debilitating autoimmune disease whose cause and mechanism remain a mystery. We recently described a T cell receptor transgenic mouse model that spontaneously develops a disease with most of the clinical, histological, and immunological features of rheumatoid arthritis in humans. Disease development in K/BxN mice is initiated by systemic T cell self-reactivity; it requires T cells, as expected, but B cells are also needed, more surprisingly. Here, we have identified the role of B cells as the secretion of arthritogenic immunoglobulins. We suggest that a similar scenario may unfold in some other arthritis models and in human patients, beginning with pervasive T cell autoreactivity and ending in immunoglobulin-provoked joint destruction.
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                Author and article information

                Journal
                Journal ID (nlm-ta): EMBO Mol Med
                Journal ID (iso-abbrev): EMBO Mol Med
                Journal ID (publisher-id): emmm
                Title: EMBO Molecular Medicine
                Publisher: WILEY-VCH Verlag (Weinheim )
                ISSN (Print): 1757-4676
                ISSN (Electronic): 1757-4684
                Publication date (Print): May 2010
                Volume: 2
                Issue: 5
                Pages: 172-187
                Affiliations
                [1 ]simpleDivision of Rheumatology, Immunology and Allergy and Partners Asthma Center, Brigham and Women's Hospital, Harvard Medical School Boston, MA, USA
                [2 ]simpleDepartments of Chemistry and Biochemistry, University of Washington Seattle, WA, USA
                [3 ]simpleThe Case Center for Proteomics, Case Western Reserve University School of Medicine Cleveland, OH, USA
                [4 ]simpleDepartment of Orthopedics, Brigham and Women's Hospital Boston, MA, USA
                [5 ]simpleInstitut de Pharmacologie Moléculaire et Cellulaire, Centre National de Recherche Scientifique and Université de Nice-Sophia-Antipolis Sophia-Antipolis, Valbonne, France
                Author notes
                * Corresponding author: Tel: +1-617-525-1016; Fax: +1-617-525-1010 E-mail: dlee@ 123456rics.bwh.harvard.edu
                ** Corresponding author: Tel: +1-617-525-1305; Fax: +1-617-525-1310 E-mail: jarm@ 123456rics.bwh.harvard.edu
                Article
                DOI: 10.1002/emmm.201000072
                PMC ID: 3058614
                PubMed ID: 20432503
                SO-VID: bf0b0ad9-7fc7-4028-aafc-166a07212ac1
                Copyright © Copyright © 2010 EMBO Molecular Medicine
                History
                Date received : 06 October 2009
                Date revision received : 10 March 2010
                Date accepted : 16 March 2010
                Categories
                Subject: Research Article

                ScienceOpen disciplines: Molecular medicine
                Keywords: arthritis,secreted phospholipase a2,autoimmunity,inflammation
                Data availability:
                ScienceOpen disciplines: Molecular medicine
                Keywords: arthritis, secreted phospholipase a2, autoimmunity, inflammation

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