Choline acetyltransferase–expressing T cells are required to control chronic viral infection
Author(s) -
Maureen A. Cox,
Gordon S. Duncan,
Gloria Lin,
Benjamin E. Steinberg,
Lisa Yu,
Dirk Brenner,
Luke N. Buckler,
Andrew Elia,
Andrew Wakeham,
Brian J. Nieman,
Carmen DominguezBrauer,
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
Publication year - 2019
Publication title -
science
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 12.556
H-Index - 1186
eISSN - 1095-9203
pISSN - 0036-8075
DOI - 10.1126/science.aau9072
Subject(s) - lymphocytic choriomeningitis , biology , choline acetyltransferase , t cell , acetylcholine , chronic infection , virus , immunity , cd8 , virology , immunology , immune system , endocrinology
ChAT-ty T cells fight viral infection The neurotransmitter acetylcholine (ACh) is involved in processes such as muscle contraction, neuron communication, and vasodilation. Along with neurons, a population of immunological T cells and B cells express the enzyme choline acetyltransferase (ChAT), which catalyzes the rate-limiting step of ACh production. However, the role of immune cell–derived ACh is unclear. Coxet al. report that the cytokine interleukin-21 (IL-21) induces ChAT expression in CD4+ and CD8+ T cells during lymphocytic choriomeningitis virus infection (see the Perspective by Hickman). T cell–specific deletion of ChAT strongly impaired vasodilation and trafficking of antiviral T cells into infected tissues, which undermined the effective control of a chronic viral infection. Thus, IL-21 plays a critical role during chronic infection. Furthermore, the findings reveal a cholinergic mechanism that can regulate immune cell migration into tissues.Science , this issue p.639 ; see also p.585
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