期刊
NATURE IMMUNOLOGY
卷 12, 期 6, 页码 478-484出版社
NATURE PUBLISHING GROUP
DOI: 10.1038/ni.2018
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资金
- National Health and Medical Research Council (Australia)
- National Institutes of Health (USA)
- National Research Foundation (Korea)
Weak T cell antigen receptor (TCR) signals from contact with self ligands act in synergy with antiapoptotic signals induced by interleukin 7 (IL-7) to promote the survival of naive T cells in a resting state. The amount of background TCR signaling in naive T cells is set by post-thymic TCR tuning and operates at an intensity just below that required to induce entry into the cell cycle. Costimulation from higher concentrations of IL-7 and other common gamma-chain cytokines can induce T cells to undergo homeostatic proliferation and conversion into cells with a memory phenotype; many of these memory phenotype cells may be the progeny of cells responding to self antigens. The molecular mechanisms that control the conversion of naive resting T cells into memory-phenotype cells TCR-dependent in normal animals are beginning to be understood.
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