Tim-3 adaptor protein Bat3 is a molecular checkpoint of T cell terminal differentiation and exhaustion
Chen Zhu(Brigham and Women's Hospital), Karen O. Dixon(Broad Institute), Kathleen Newcomer(Harvard University), Guangxiang Gu(Brigham and Women's Hospital), Sheng Xiao(Celsius Therapeutics (United States)), Sarah Zaghouani(Brigham and Women's Hospital), Markus A. Schramm(Brigham and Women's Hospital), Chao Wang(Brigham and Women's Hospital), Huiyuan Zhang(Brigham and Women's Hospital), Kouichiro Goto(Ontario Institute for Cancer Research), Elena Christian(University of Massachusetts Boston), Manu Rangachari(Université Laval), Orit Rosenblatt-Rosen(University of Massachusetts Boston), Hitoshi Okada(Kindai University), Tak W. Mak(Ontario Institute for Cancer Research), Meromit Singer(Broad Institute), Aviv Regev(Broad Institute), Vijay K. Kuchroo(Broad Institute)
Cited by 41Open Access
Abstract
T cells revealed up-regulation of dysfunction-associated genes, concomitant with down-regulation of genes associated with T cell effector function, suggesting that absence of Bat3 can trigger T cell dysfunction even under highly proinflammatory autoimmune conditions.
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