Choline acetyltransferase–expressing T cells are required to control chronic viral infection

Maureen A. Cox, Gordon S. Duncan, Gloria H.Y. Lin, Benjamin E. Steinberg, Lisa X. Yu, Dirk Brenner, Luke N. Buckler, Andrew J. Elia, Andrew C. Wakeham, Brian Nieman, Carmen Dominguez-Brauer, Alisha R. Elford, Kyle T. Gill, Shawn P. Kubli, Jillian Haight, Thorsten Berger, Pamela S. Ohashi, Kevin J. Tracey, Peder S. Olofsson, Tak W. Mak*

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

90 Citations (Scopus)


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.

Original languageEnglish
Pages (from-to)639-644
Number of pages6
Issue number6427
Publication statusPublished - 8 Feb 2019


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