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Here, we show that effector and memory T cells from mice expressing a dominant negative E3\u2010inactive c\u2010IAP2 (c\u2010IAP2<jats:sup>H570A<\/jats:sup>) have impaired signaling downstream of 4\u20101BB. When infected with lymphocytic choriomeningitis virus, unlike mice in which c\u2010IAPs were acutely downregulated by c\u2010IAP antagonists, the primary response of c\u2010IAP2<jats:sup>H570A<\/jats:sup> mice was normal. However, the number of antigen\u2010specific CD8<jats:sup>+<\/jats:sup> but not CD4<jats:sup>+<\/jats:sup> T cells declined more rapidly and to a greater extent in c\u2010IAP2<jats:sup>H570A<\/jats:sup> mice than in WT controls. Studies with T\u2010cell adoptive transfer demonstrated that the enhanced decay of memory cells was T\u2010cell intrinsic. Thus, c\u2010IAP E3 activity is required for 4\u20101BB coreceptor signaling and maintenance of CD8<jats:sup>+<\/jats:sup> T\u2010cell memory.<\/jats:p>","DOI":"10.1002\/eji.201445342","type":"journal-article","created":{"date-parts":[[2015,6,19]],"date-time":"2015-06-19T10:07:34Z","timestamp":1434708454000},"page":"2672-2682","source":"Crossref","is-referenced-by-count":16,"title":["c\u2010IAP ubiquitin protein ligase activity is required for 4\u20101BB signaling and CD8<sup>+<\/sup> memory T\u2010cell survival"],"prefix":"10.1002","volume":"45","author":[{"given":"Maria Letizia","family":"Giardino Torchia","sequence":"first","affiliation":[{"name":"Laboratory of Immune Cell Biology National Cancer Institute National Institutes of Health  Bethesda MD USA"}],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Ivana","family":"Munitic","sequence":"additional","affiliation":[{"name":"Laboratory of Immune Cell Biology National Cancer Institute National Institutes of Health  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