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To evaluate the contribution of different Fas signalling pathways, mice overexpressing FLIP<jats:sub>L<\/jats:sub>, Bcl\u2010x<jats:sub>L<\/jats:sub>, a kinase\u2010deficient form of RIP (RIP\u0394kin) or combinations thereof were generated by retroviral gene transfer of haematopoietic stem cells. Such mice did not show overt abnormalities in haematopoietic development, defects in thymic deletion, accumulation of double\u2010negative T cells or signs of autoimmunity. Fas\u2010mediated death of mitogen\u2010activated T cells was caspase dependent and could be blocked by FLIP<jats:sub>L<\/jats:sub> overexpression only with the minor involvement of Bcl\u2010x<jats:sub>L<\/jats:sub> or RIP\u0394kin inhibitable pathways. Fas\u2010mediated death of resting CD4<jats:sup>+<\/jats:sup> and CD8<jats:sup>+<\/jats:sup> T cells was mainly caspase dependent but could only partly be blocked by FLIP<jats:sub>L<\/jats:sub> overexpression. Both Bcl\u2010x<jats:sub>L<\/jats:sub> or RIP\u0394kin expression resulted in partial protection of CD8<jats:sup>+<\/jats:sup> T cells against Fas\u2010mediated cell death. These results indicate that yet uncharacterized signalling pathways from the Fas receptor are critically involved in lymphoproliferative and autoimmune disease observed in <jats:italic>lpr<\/jats:italic> mice and autoimmune lymphoproliferative syndrome patients.<\/jats:p>","DOI":"10.1111\/j.1365-3083.2007.01957.x","type":"journal-article","created":{"date-parts":[[2007,7,31]],"date-time":"2007-07-31T16:03:57Z","timestamp":1185897837000},"page":"410-421","update-policy":"http:\/\/dx.doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":4,"title":["Participation of FLIP, RIP and Bcl\u2010x<sub>L<\/sub> in Fas\u2010mediated T\u2010cell Death"],"prefix":"10.1111","volume":"66","author":[{"given":"M.","family":"Djerbi","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"M. 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