期刊
JOURNAL OF IMMUNOLOGY
卷 180, 期 1, 页码 156-162出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.180.1.156
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资金
- NATIONAL INSTITUTE OF ALLERGY AND INFECTIOUS DISEASES [P01AI035296, T32AI007313] Funding Source: NIH RePORTER
- NIAID NIH HHS [T32 AI07313, P01 AI35296] Funding Source: Medline
To investigate the role of TCR signaling in the exit of CD4(+) T cells from cell cycle, we took advantage of a low frequency TEa T cell adoptive transfer technique as well as the Y-Ae mAb to interrupt Ag/MHC recognition before the completion of clonal expansion. Termination of TCR signaling after 36 h of Ag exposure caused an immediate reduction in cell size and deceleration of G(1)-> SG(2)M phase cell cycle progression. As a consequence, clonal expansion in the absence of durable TCR signaling decreased by two-thirds. Thus, CD4(+) T cells scan for the presence Ag throughout their clonal expansion response, and continuously adjust their rate of cell growth and G(1)-> S phase transition to match their intensity of TCR signaling.
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