| Literature DB >> 30733420 |
Maureen A Cox1, Gordon S Duncan1, Gloria H Y Lin1, Benjamin E Steinberg1,2, Lisa X Yu3, Dirk Brenner1,4,5, Luke N Buckler1, Andrew J Elia1, Andrew C Wakeham1, Brian Nieman3,6, Carmen Dominguez-Brauer1, Alisha R Elford1, Kyle T Gill1, Shawn P Kubli1, Jillian Haight1, Thorsten Berger1, Pamela S Ohashi1,7, Kevin J Tracey8, Peder S Olofsson8,9, Tak W Mak10,6,7,11.
Abstract
Although widely studied as a neurotransmitter, T cell-derived acetylcholine (ACh) has recently been reported to play an important role in regulating immunity. However, the role of lymphocyte-derived ACh in viral infection is unknown. Here, we show that the enzyme choline acetyltransferase (ChAT), which catalyzes the rate-limiting step of ACh production, is robustly induced in both CD4+ and CD8+ T cells during lymphocytic choriomeningitis virus (LCMV) infection in an IL-21-dependent manner. Deletion of Chat within the T cell compartment in mice ablated vasodilation in response to infection, impaired the migration of antiviral T cells into infected tissues, and ultimately compromised the control of chronic LCMV clone 13 infection. Our results reveal a genetic proof of function for ChAT in T cells during viral infection and identify a pathway of T cell migration that sustains antiviral immunity.Entities:
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Year: 2019 PMID： 30733420 PMCID： PMC7181845 DOI： 10.1126/science.aau9072
Source DB: PubMed Journal: Science ISSN： 0036-8075 Impact factor: 47.728