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

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The costimulation-regulated duration of PKB activation controls T cell longevity.

A brief antigenic stimulus can promote T cell proliferation, but the duration and nature of intracellular signals required for survival are unclear. Here we show that in the absence of OX40 costimulation, antigen-activated CD4+ cells are short-lived because the activity of protein kinase B ( PKB; also known as Akt) is not maintained over time. Activated T cells that express a dominant-negative variant of PKB also undergo apoptosis, reproducing the OX40-deficient phenotype. In contrast, an active form of PKB prevents downregulation of antiapoptotic proteins in OX40-deficient T cells, rescues antigen-induced cell survival in vivo, and controls inflammation in recall responses. Thus, sustained and periodic PKB signaling has an integral role in regulating T cell longevity.[1]

References

  1. The costimulation-regulated duration of PKB activation controls T cell longevity. Song, J., Salek-Ardakani, S., Rogers, P.R., Cheng, M., Van Parijs, L., Croft, M. Nat. Immunol. (2004) [Pubmed]
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