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Hoffmann, R. A wiki for the life sciences where authorship matters. Nature Genetics (2008)
 
 
 
 
 

CD28 and apoptosis.

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.[1]

References

  1. CD28 and apoptosis. Boise, L.H., Noel, P.J., Thompson, C.B. Curr. Opin. Immunol. (1995) [Pubmed]
 
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