{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,14]],"date-time":"2026-05-14T08:19:33Z","timestamp":1778746773841,"version":"3.51.4"},"reference-count":23,"publisher":"Wiley","issue":"1pt2","license":[{"start":{"date-parts":[[2008,9,17]],"date-time":"2008-09-17T00:00:00Z","timestamp":1221609600000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Immunology"],"published-print":{"date-parts":[[2009,9]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p>Concanavalin A (Con A)\u2010induced hepatitis is a T\u2010cell\u2010mediated murine experimental model of autoimmune hepatitis. Mice lacking V\u03b114 NKT cells were found to be less sensitive to this hepatitis and the MRL\/Mp\u2010<jats:italic>Fas<\/jats:italic><jats:sup><jats:italic>lpr\/lpr<\/jats:italic><\/jats:sup> (MRL\/lpr; i.e. Fas deficient) mice were also less sensitive. We report herein that MRL\/Mp\u2010<jats:italic>Fas<\/jats:italic><jats:sup><jats:italic>lpr\/lpr<\/jats:italic><\/jats:sup>\u2010<jats:italic>Sap<\/jats:italic><jats:sup><jats:italic>rpl\/\u2212<\/jats:italic><\/jats:sup> (MRL\/lpr\/rpl) mice lack V\u03b114 NKT cells and are deficient in the Fas antigen but sensitive to Con A\u2010induced hepatitis. The signaling lymphocytic activation molecule (SLAM)\u2010associated protein (SAP) is an adaptor molecule containing a Src homology 2 (SH2) domain. We previously reported new mutant mice found among MRL\/lpr mice and revealed that SAP deficiency led to the regression of autoimmune phenotypes in mutant MRL\/lpr\/rpl mice. It was also revealed that CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells were effector cells and that blockade of 2B4, one of the SLAM family receptors, inhibited the induction of hepatitis in MRL\/lpr\/rpl mice. These data suggest that signals mediated by molecules other than SAP from 2B4 in T cells played important roles in the induction of hepatitis in MRL\/lpr\/rpl mice.<\/jats:p>","DOI":"10.1111\/j.1365-2567.2008.02936.x","type":"journal-article","created":{"date-parts":[[2008,9,17]],"date-time":"2008-09-17T12:21:32Z","timestamp":1221654092000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Role of 2B4\u2010mediated signals in the pathogenesis of a murine hepatitis model independent of Fas and V\u03b114 NKT 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