Open AccessTim-3 on CD4+T cells is associated with pathology in experimental autoimmune encephalomyelitis of mouse
Author(s) -
Qi Guo
Publication year - 2021
Publication title -
european journal of inflammation
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.219
H-Index - 20
eISSN - 2058-7392
pISSN - 1721-727X
DOI - 10.1177/20587392211030149
Subject(s) - experimental autoimmune encephalomyelitis , multiple sclerosis , immunology , immune system , inflammation , autoimmune disease , pathogenesis , autoimmunity , encephalomyelitis , flow cytometry , t cell , experimental pathology , medicine , biology , antibody , cell culture , genetics
Experimental autoimmune encephalomyelitis (EAE) is a reliable model to study the pathogenesis of Multiple sclerosis (MS), which is a progressive autoimmune-mediated inflammation of the central nervous system (CNS). Tim-3 is one of the crucial immune checkpoints in immune tolerance. We investigated the impact of Tim3 in EAE by the anti-Tim3 antibody and detected the immune cell and inflammation through flow cytometry and ELISA. In this study we found that CD4 T cells express low levels of Tim-3 in EAE mice. Tim-3 suppression exacerbated the disease progression in EAE mice. Furthermore, the Galectin-9/Tim-3 pathway promoted the apoptosis of CD4 T cells and inhibited the differentiation of Th17 in EAE mice. Our study unravels the anti-inflammatory Galectin-9/Tim-3 pathway in EAE mice and provides a potential therapeutic target for EAE and MS treatment.