國家衛生研究院 NHRI:Item 3990099045/12455

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Title:	Intracellular galectin-9 enhances proximal TCR signaling and potentiates autoimmune diseases
Authors:	Chen, HY;Wu, YF;Chou, FC;Wu, YH;Yeh, LT;Lin, KI;Liu, FT;Sytwu, HK
Contributors:	National Institute of Infectious Diseases and Vaccinology
Abstract:	Galectin-9 is a risk gene in inflammatory bowel disease. By transcriptomic analyses of ileal biopsies and PBMCs from inflammatory bowel disease patients, we identified a positive correlation between galectin-9 expression and colitis severity. We observed that galectin-9-deficient T cells were less able to induce T cell-mediated colitis. However, several mouse-based studies reported that galectin-9 treatment induces T cell apoptosis and ameliorates autoimmune diseases in an exogenously modulated manner, indicating a complicated regulation of galectin-9 in T cells. We found that galectin-9 is expressed mainly inside T cells, and its secreted form is barely detected under physiological conditions. Endogenous galectin-9 was recruited to immune synapses upon T cell activation. Moreover, proximal TCR signaling was impaired in galectin-9-deficient T cells, and proliferation of these cells was decreased through an intracellularly modulated manner. Th17 cell differentiation was downregulated in galectin-9-deficient T cells, and this impairment can be rescued by strong TCR signaling. Taken together, these findings suggest that intracellular galectin-9 is a positive regulator of T cell activation and modulates the pathogenesis of autoimmune diseases.
Date:	2020-03-01
Relation:	Journal of Immunology. 2020 Mar 1;204(5):1158-1172.
Link to:	http://dx.doi.org/10.4049/jimmunol.1901114
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0022-1767&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000514841600009
Cited Times(Scopus):	https://www.scopus.com/inward/record.url?partnerID=HzOxMe3b&scp=85079872060
Appears in Collections:	[Huey-Kang Sytwu] Periodical Articles

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