期刊
IMMUNITY
卷 38, 期 5, 页码 881-895出版社
CELL PRESS
DOI: 10.1016/j.immuni.2013.02.008
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资金
- Japan Society for the Promotion of Science (JSPS)
- PRESTO from the Japan Science and Technology Agency (JST)
- Ministry of Education, Culture, Sports, Science and Technology of Japan
- ERATO
- Takayanagi Osteonetwork Project from the JST
- NIH [AI 066128, AI40127, AI84167]
- Takeda Life Science Foundation
- Mochida Memorial Foundation for Medical and Pharmaceutical Research
- JSPS Research Fellowships for Young Scientists
- Grants-in-Aid for Scientific Research [23590565] Funding Source: KAKEN
T cell receptor (TCR) signaling driven by interaction of the TCR with specific complexes of self-peptide and the major histocompatibility complex determines T cell fate in thymic development. However, the signaling pathway through which TCR signal strength regulates distinct T cell lineages remains unknown. Here we have used mice lacking the endoplasmic reticulum Ca2+ sensors stromal interaction molecule 1 (STIM1) and STIM2 to show that STIM-induced store-operated Ca2+ entry is not essential for thymic development of conventional TCR alpha beta(+) T cells but is specifically required for the development of agonist-selected T cells (regulatory T cells, invariant natural killer T cells, and TCR alpha beta(+) CD8 alpha alpha(+) intestinal intraepithelial lymphocytes). The severe impairment of agonist-selected T cell development is mainly due to a defect in interleukin-2 (IL-2) or IL-15 signaling. Thus, STIM1 and STIM2-mediated store-operated Ca2+ influx, leading to efficient activation of NFAT (nuclear factor of activated T cells), is critical for the postselection maturation of agonist-selected T cells.
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