期刊
IMMUNITY
卷 27, 期 2, 页码 281-295出版社
CELL PRESS
DOI: 10.1016/j.immuni.2007.07.010
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资金
- NIAID NIH HHS [T32 AI055403, R01 AI 066232-01, R01 AI056322, R01 AI057485-01, R01 AI054661, P01 AI22295, R01 AI066232, R01 AI056322-01, R01 AI066232-01, P01 AI022295, R01 AI057485] Funding Source: Medline
As acute infections resolve, effector CD8(+) T cells differentiate into interleukin-7 receptor(lo) (IL-7R(lo)) short-lived effector cells (SLECs) and IL-7R(hi) memory precursor effector cells (MPECs) capable of generating long-lived memory CD8(+) T cells. By using another SLEC marker, KLRG1, we found that KLRG1(hi) effector cells began appearing early during infection and were committed to downregulating IL-7R. Unlike IL-7R(hi) MPECs, KLRG1(hi) IL-7R(lo) SLECs relied on IL-15, but I L-15 could not sustain their long-term maintenance or homeostatic turnover. The decision between SLEC and MPEC fates was regulated by the amount of inflammatory cytokines (i.e., IL-12) present during T cell priming. According to the amount of inflammation, a gradient of T-bet was created in which high T-bet expression induced SLECs and low expression promoted MPECs. These results elucidate a mechanism by which the innate immune system sets the relative amounts of a lineage-determining transcription factor in activated CD8(+) T cells and, correspondingly, regulates their memory cell potential.
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