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CD28 and apoptosis.

L H Boise·P J Noel·C B Thompson
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Abstract

Until recently, it was thought that signal transduction through CD28 and the related molecule CTLA4 prevented the induction of anergy in T cells activated through the TCR. This hypothesis has been suggested as an explanation for how soluble forms of CTLA4, which bind the CD28/CTLA4 ligands B7-1 and B7-2, can prevent graft rejection. Recent reports suggest that another function of CD28 costimulation is the regulation of T-cell survival. CD28 not only enhances IL-2 production, which can act as an extrinsic regulator of cell survival, but also augments the expression of the intrinsic survival factor Bcl-xL. In contrast, CTLA4-mediated signal transduction has been reported to induce cell death in previously activated T cells. These data suggest that B7-1/B7-2 signaling not only controls cell proliferation and T-helper cell subset selection, but also T-cell survival.

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AnimalsApoptosisCD28 AntigensHumansSignal TransductionT-LymphocytesJournal ArticleResearch Support, U.S. Gov't, P.H.S.Review

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L H Boise, P J Noel, C B Thompson. 1995. CD28 and apoptosis.. https://doi.org/10.1016/0952-7915(95)80067-0

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