PMID:14730361

Citation	Song, J, Salek-Ardakani, S, Rogers, PR, Cheng, M, Van Parijs, L and Croft, M (2004) The costimulation-regulated duration of PKB activation controls T cell longevity. Nat. Immunol. 5:150-8
Abstract	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.
Links	PubMed Online version:10.1038/ni1030
Keywords	Animals; Apoptosis; Cell Division; Cell Survival; Inflammation/enzymology; Inflammation/immunology; Mice; Mice, Knockout; Mice, Transgenic; Protein-Serine-Threonine Kinases; Proto-Oncogene Proteins/genetics; Proto-Oncogene Proteins/metabolism; Proto-Oncogene Proteins c-akt; Receptors, Antigen, T-Cell/genetics; Receptors, OX40; Receptors, Tumor Necrosis Factor/deficiency; Receptors, Tumor Necrosis Factor/genetics; Signal Transduction; T-Lymphocytes/cytology; T-Lymphocytes/enzymology; T-Lymphocytes/immunology
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