期刊
CELL REPORTS
卷 14, 期 5, 页码 1218-1231出版社
CELL PRESS
DOI: 10.1016/j.celrep.2016.01.002
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资金
- NIH [U19 AI090019, R01 AG015043, U19 AI057266, U01 AI089859-IOF, I01 BX001669, R01 AI108891, R01 AR042547, R01 EY011916, R01 AI044142, R01 AI108906, R01 HL117913, P01 HL058000]
- VA [5I01BX001669-02, 550140, 5I01BX001669-04, 731709] Funding Source: Federal RePORTER
In an immune response, CD4(+) T cells expand into effector T cells and then contract to survive as long-lived memory cells. To identify age-associated defects in memory cell formation, we profiled activated CD4(+) T cells and found an increased induction of the ATPase CD39 with age. CD39(+) CD4(+) T cells resembled effector T cells with signs of metabolic stress and high susceptibility to undergo apoptosis. Pharmacological inhibition of ATPase activity dampened effector cell differentiation and improved survival, suggesting that CD39 activity influences T cell fate. Individuals carrying a low-expressing CD39 variant responded better to vaccination with an increase in vaccine-specific memory T cells. Increased inducibility of CD39 after activation may contribute to the impaired vaccine response with age.
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