Open AccessGIT2 deficiency attenuates concanavalin A‐induced hepatitis in mice
Author(s) -
Hao Yu-E,
He Dong-Fang,
Yin Rong-Hua,
Chen Hui,
Wang Jian,
Wang Shao-Xia,
Zhan Yi-Qun,
Ge Chang-Hui,
Li Chang-Yan,
Yu Miao,
Yang Xiao-Ming
Publication year - 2015
Publication title -
febs open bio
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.718
H-Index - 31
ISSN - 2211-5463
DOI - 10.1016/j.fob.2015.08.005
Subject(s) - biology , microbiology and biotechnology , receptor , signal transduction , concanavalin a , cytokine , in vitro , immunology , biochemistry
G protein‐coupled receptor kinase interactor 2 (GIT2) is a signaling scaffold protein involved in regulation of cytoskeletal dynamics and the internalization of G protein‐coupled receptors (GPCRs). The short‐splice form of GIT2 is expressed in peripheral T cells and thymocytes. However, the functions of GIT2 in T cells have not yet been determined. We show that treatment with Con A in a model of polyclonal T‐lymphocyte activation resulted in marked inhibitions in the intrahepatic infiltration of inflammatory cells, cytokine response and acute liver failure in Git2 −/− mice. CD4 + T cells from Git2 −/− mice showed significant impairment in proliferation, cytokine production and signal transduction upon TCR‐stimulated activation. Our results suggested that GIT2 plays an important role in T‐cell function in vivo and in vitro .