期刊
NATURE IMMUNOLOGY
卷 5, 期 2, 页码 150-158出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni1030
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- NCI NIH HHS [CA 91827] Funding Source: Medline
- NIAID NIH HHS [AI 50498] Funding Source: Medline
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.
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