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- W4313349733 abstract "Abstract As acute infections resolve, most effector CD8+ T cells die, while some persist and become memory T cells. Recent work showed that subsets of effector CD8+ T cells, identified by reciprocal expression of KLRG1 and CD127, have different lifespans. Similar to previous reports, we found that effector CD8+ T cells reported to have a longer lifespan (i.e. KLRG1lo CD127hi) have increased levels of Bcl-2 compared to their shorter lived KLRG1hi CD127lo counterparts. Surprisingly, we found that these effector KLRG1lo CD127hi CD8+ T cells also had increased levels of Bim compared to KLRG1hi CD127lo cells. Similarly, central memory CD8+ T cells (TCM) expressed higher levels of Bim and Bcl-2 than did effector memory CD8+ T cells (TEM). Using both pharmacologic and genetic approaches, we found that survival of both subsets of effector and memory CD8+ T cells required Bcl-2 to combat the pro-apoptotic activity of Bim. Interestingly, inhibition or absence of Bcl-2 led to significantly decreased expression of Bim in surviving effector and memory T cells. In addition, manipulation of Bcl-2 levels by IL-7 or IL-15 also affected expression of Bim in effector CD8+ T cells. Finally, we found that Bim levels were significantly increased in effector CD8+ T cells lacking Bax and Bak. Together, these data indicate that cells having the highest levels of Bim are selected against during contraction of the response and that Bcl-2 determines the level of Bim that effector and memory T cells can tolerate." @default.
- W4313349733 created "2023-01-06" @default.
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- W4313349733 date "2011-04-01" @default.
- W4313349733 modified "2023-09-27" @default.
- W4313349733 title "BCL-2 allows effector and memory CD8+ T cells to tolerate higher expression of BIM (104.19)" @default.
- W4313349733 doi "https://doi.org/10.4049/jimmunol.186.supp.104.19" @default.
- W4313349733 hasPublicationYear "2011" @default.
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