{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,1]],"date-time":"2026-10-01T21:45:27Z","timestamp":1790891127655,"version":"4.1.0"},"reference-count":57,"publisher":"Oxford University Press (OUP)","issue":"1","license":[{"start":{"date-parts":[[2003,7,1]],"date-time":"2003-07-01T00:00:00Z","timestamp":1057017600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2003,7,1]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:p>Fas-associated death domain (FADD) is a death domain containing cytoplasmic adapter molecule required for the induction of apoptosis by death receptors. Paradoxically, FADD also plays a crucial role in the development and proliferation of T cells. Using T cells from mice expressing a dominant negative form of FADD (FADDdd), activation with anti-TCR Ab and costimulation or exogenous cytokines is profoundly diminished. This is also seen in wild-type primary T cells transduced with the same transgene, demonstrating that FADD signaling is required in normally differentiated T cells. The defective proliferation does not appear to be related to the early events associated with TCR stimulation. Rather, with a block in FADD signaling, stimulated T cells exhibit a high rate of cell death corresponding to the initiation of cell division. Although CD4 T cells exhibit a moderate deficiency, this effect is most profound in CD8 T cells. In vivo, the extent of this defective accumulation is most apparent; lymphocytic choriomenigitis virus-infected FADDdd-expressing mice completely fail to mount an Ag-specific response. These results show that, in a highly regulated fashion, FADD, and most likely caspases, can transduce either a signal for survival or one that leads directly to apoptosis and that the balance between these opposing outcomes is crucial to adaptive immunity.<\/jats:p>","DOI":"10.4049\/jimmunol.171.1.247","type":"journal-article","created":{"date-parts":[[2014,4,20]],"date-time":"2014-04-20T19:28:08Z","timestamp":1398022088000},"page":"247-256","source":"Crossref","is-referenced-by-count":56,"title":["The Requirements for Fas-Associated Death Domain Signaling in Mature T Cell Activation and Survival"],"prefix":"10.1093","volume":"171","author":[{"given":"Daniel R","family":"Beisner","sequence":"first","affiliation":[{"name":"Molecular Biology Section, Division of Biological Sciences, University of California , San Diego, CA 92093"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Isaac H","family":"Chu","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Biochemistry, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Adrian F","family":"Arechiga","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Biochemistry, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Stephen M","family":"Hedrick","sequence":"additional","affiliation":[{"name":"Molecular Biology Section, Division of Biological Sciences, University of California , San Diego, CA 92093"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Craig M","family":"Walsh","sequence":"additional","affiliation":[{"name":"Department of Molecular Biology and Biochemistry, University of California , Irvine, CA 92697"},{"name":"Cancer Research Institute, University of California , Irvine, CA 92697"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2003,7,1]]},"reference":[{"key":"2026020210161570100_R1","first-page":"1747","volume-title":"J. 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