期刊
CELL REPORTS
卷 30, 期 10, 页码 3448-+出版社
CELL PRESS
DOI: 10.1016/j.celrep.2020.02.054
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资金
- NIH [R01AR068249, R01AR071277, R01AR074285, R01HL130191, R01AI148690, K01AR067250]
- Thomas E. Starzl Postdoctoral Fellowship in Transplantation Biology
- National Cancer Institute of Canada Terry Fox Program [015005]
- Canadian Institute of Health Research [9862]
Efficient Ca2+ flux induced during cognate T cell activation requires signaling the T cell receptor (TCR) and unidentified G-protein-coupled receptors (GPCRs). T cells express the neurokinin-1 receptor (NK1R), a GPCR that mediates Ca2+ flux in excitable and non-excitable cells. However, the role of the NK1R in TCR signaling remains unknown. We show that the NK1R and its agonists, the neuropeptides substance P and hemokinin-1, co-localize within the immune synapse during cognate activation of T cells. Simultaneous TCR and NK1R stimulation is necessary for efficient Ca2+ flux and Ca2+-dependent signaling that sustains the survival of activated T cells and helper 1 (Th1) and Th17 bias. In a model of contact dermatitis, mice with T cells deficient in NK1R or its agonists exhibit impaired cellular immunity, due to high mortality of activated T cells. We demonstrate an effect of the NK1R in T cells that is relevant for immunotherapies based on pro-inflammatory neuropeptides and its receptors.
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