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Nat Immunol. 2004 Feb;5(2):150-8. Epub 2004 Jan 18.

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

Author information

1
Division of Molecular Immunology, La Jolla Institute for Allergy and Immunology, San Diego, CA 92121, USA.

Erratum in

  • Nat Immunol. 2004 Nov;5(11):1190.
  • Nat Immunol. 2005 Feb;6(2):219.

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.

PMID:
14730361
DOI:
10.1038/ni1030
[Indexed for MEDLINE]

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