{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,2,10]],"date-time":"2026-02-10T03:47:03Z","timestamp":1770695223341,"version":"3.49.0"},"reference-count":29,"publisher":"Wiley","issue":"6","license":[{"start":{"date-parts":[[2005,12,12]],"date-time":"2005-12-12T00:00:00Z","timestamp":1134345600000},"content-version":"vor","delay-in-days":3116,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Arthritis &amp; Rheumatism"],"published-print":{"date-parts":[[1997,6]]},"abstract":"<jats:title>Abstract<\/jats:title><jats:p><jats:italic>Objective.<\/jats:italic> To characterize Fas antigen expression on the cell surface, and to determine the effect of this expression in rheumatic diseases using a newly established <jats:italic>gld<\/jats:italic>\u2010congenic MRL strain of mice (MRL\/<jats:italic>gld<\/jats:italic>), which is defective in its functional Fas ligand (Fas\u2010L).<\/jats:p><jats:p><jats:italic>Methods.<\/jats:italic> Flow cytometric analyses of lymphoid cells and macrophages were performed using anti\u2010Fas and other cell surface markers. Histopathologic manifestations were examined using immunochemistry and light and electron microscopy. Serum levels of IgG and anti\u2010DNA antibodies were measured by single radial immunodiffusion and enzyme\u2010linked immunosorbent assay, respectively.<\/jats:p><jats:p><jats:italic>Results.<\/jats:italic> MRL\/<jats:italic>gld<\/jats:italic> mice developed systemic lymph\u2010adenopathy with an accumulation of Thy1.2+, B220+ and CD4\u2010, CD8\u2010 T cells, which both express the Fas antigen. Splenic B cells positive for surface IgM and\/or surface IgD, and resident peritoneal macrophages exhibited up\u2010regulated expression of the Fas antigen, at much higher levels than those observed in MRL\/MpJ\u2010+\/+ (MRL\/+) mice. Forms of rheumatic disease were observed in these mice, although not in C3H\/HeJ\u2010<jats:italic>gld\/gld<\/jats:italic> mice. These forms included diffuse glomerulonephritis, granulomatous arteritis, and arthritis, and were associated with the infiltration of mononuclear cells expressing the Fas antigen. Serum levels of IgG and anti\u2010DNA antibodies were significantly increased in MRL\/<jats:italic>gld<\/jats:italic> mice compared with MRL\/+ mice.<\/jats:p><jats:p><jats:italic>Conclusion.<\/jats:italic> Rheumatic disease was generated by the <jats:italic>gld<\/jats:italic> gene in mice with an MRL background, as it is by the <jats:italic>lpr<\/jats:italic> gene, which is a Fas deletion mutant, associated with autoimmune traits. Rheumatic disease in this MRL strain was initiated by an incapacity for Fas\/Fas\u2010L\u2010induced apoptosis, resulting in the development of autoimmunity and allowing for a persistent immune response in the affected lesions.<\/jats:p>","DOI":"10.1002\/art.1780400610","type":"journal-article","created":{"date-parts":[[2007,2,14]],"date-time":"2007-02-14T12:42:54Z","timestamp":1171456974000},"page":"1054-1063","source":"Crossref","is-referenced-by-count":54,"title":["Rheumatic diseases in an MRL strain of mice with a deficit in the functional Fas ligand"],"prefix":"10.1002","volume":"40","author":[{"given":"Mituko 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