{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T12:46:29Z","timestamp":1791117989821,"version":"4.1.0"},"reference-count":191,"publisher":"Wiley","issue":"1","license":[{"start":{"date-parts":[[2011,10,21]],"date-time":"2011-10-21T00:00:00Z","timestamp":1319155200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Immunological Reviews"],"published-print":{"date-parts":[[2011,11]]},"abstract":"<jats:p>\n                    <jats:bold>Summary:\u2002<\/jats:bold>\n                    GITR [glucocorticoid inducible tumor necrosis factor receptor (TNFR)\u2010related protein] and 4\u20101BB are costimulatory TNFR family members that are expressed on regulatory and effector T cells as well as on other cells of the immune system. Here we discuss the role of GITR and 4\u20101BB on T cells during viral infections and in cancer immunotherapy. Systemic treatment with agonistic anti\u20104\u20101BB antibody leads to a number of immune system abnormalities, and clinical trials of anti\u20104\u20101BB have been terminated. However, other modes of 4\u20101BB ligation may be less toxic. To date, similar toxicities have not been reported for anti\u2010GITR treatment of mice, although anti\u2010GITR antibodies can exacerbate mouse autoimmune models. Intrinsic effects of GITR and 4\u20101BB on effector T cells appear to predominate over their effects on other cell types in some models. Despite their similarities in enhancing T\u2010cell survival, 4\u20101BB and GITR are clearly not redundant, and both pathways are required for maximal CD8\n                    <jats:sup>+<\/jats:sup>\n                    T\u2010cell responses and mouse survival following severe respiratory influenza infection. GITR uses TNFR\u2010associated factor (TRAF) 2 and TRAF5, whereas 4\u20101BB recruits TRAF1 and TRAF2 to mediate survival signaling in T cells. The differential use of signaling adapters combined with their differential expression may explain the non\u2010redundant roles of GITR and 4\u20101BB in the immune system.\n                  <\/jats:p>","DOI":"10.1111\/j.1600-065x.2011.01063.x","type":"journal-article","created":{"date-parts":[[2011,10,21]],"date-time":"2011-10-21T09:06:14Z","timestamp":1319187974000},"page":"197-217","source":"Crossref","is-referenced-by-count":108,"title":["T\u2010cell intrinsic effects of GITR and 4\u20101BB during viral infection and cancer immunotherapy"],"prefix":"10.1111","volume":"244","author":[{"given":"Laura M.","family":"Snell","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Gloria H. 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