期刊
IMMUNITY
卷 52, 期 2, 页码 313-+出版社
CELL PRESS
DOI: 10.1016/j.immuni.2020.01.018
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资金
- Netherlands Organization for Scientific Research (NWO) [864.12.013]
- Elite Network of Bavaria, Bavarian State Ministry of Science and the Arts [N-LW-2016-370]
- Technical University of Munich
- German Research Foundation (DFG) [RO 4120/2-1, SFB1160]
T cell responses upon infection display a remarkably reproducible pattern of expansion, contraction, and memory formation. If the robustness of this pattern builds entirely on signals derived from other cell types or if activated T cells themselves contribute to the orchestration of these population dynamics-akin to bacterial quorum regulation-is unclear. Here, we examined this question using time-lapse microscopy, genetic perturbation, bioinformatic predictions, and mathematical modeling. We found that ICAM-1-mediated cell clustering enabled CD8(+) T cells to collectively regulate the balance between proliferation and apoptosis. Mechanistically, T cell expressed CD80 and CD86 interacted with the receptors CD28 and CTLA-4 on neighboring T cells; these interactions fed two nested antagonistic feedback circuits that regulated interleukin 2 production in a manner dependent on T cell density as confirmed by in vivo modulation of this network. Thus, CD8(+) T cell-population-intrinsic mechanisms regulate cellular behavior, thereby promoting robustness of population dynamics.
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