| Literature DB >> 25282159 |
Lilian L Nohara1, Hongjian Xu1, Samuel Bertin2, Yukari Aoki-Nonaka2,3, Petrus Rudolf de Jong2, Shawna R Stanwood1, Sonal Srikanth4, Jihyung Lee2, Keith To2, Lior Abramson2, Timothy Yu2, Tiffany Han2, Ranim Touma5, Xiangli Li2, José M González-Navajas2, Scott Herdman2, Maripat Corr2, Guo Fu6,7, Hui Dong2, Yousang Gwack4, Alessandra Franco5, Wilfred A Jefferies1, Eyal Raz2.
Abstract
TRPV1 is a Ca(2+)-permeable channel studied mostly as a pain receptor in sensory neurons. However, its role in other cell types is poorly understood. Here we found that TRPV1 was functionally expressed in CD4(+) T cells, where it acted as a non-store-operated Ca(2+) channel and contributed to T cell antigen receptor (TCR)-induced Ca(2+) influx, TCR signaling and T cell activation. In models of T cell-mediated colitis, TRPV1 promoted colitogenic T cell responses and intestinal inflammation. Furthermore, genetic and pharmacological inhibition of TRPV1 in human CD4(+) T cells recapitulated the phenotype of mouse Trpv1(-/-) CD4(+) T cells. Our findings suggest that inhibition of TRPV1 could represent a new therapeutic strategy for restraining proinflammatory T cell responses.Entities:
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Year: 2014 PMID： 25282159 PMCID： PMC4843825 DOI： 10.1038/ni.3009
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606