國家衛生研究院 NHRI:Item 3990099045/12352

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Please use this identifier to cite or link to this item: http://ir.nhri.org.tw/handle/3990099045/12352

Title:	Endogenous galectin-9 potentiates CD4(+)T cell activation through promoting TCR downstream signaling
Authors:	Chen, HY;Chou, FC;Wu, YH;Yeh, LT;Liu, FT;Sytwu, HK
Contributors:	National Institute of Infectious Diseases and Vaccinology
Abstract:	Galectin-9, ab-galactoside-binding protein, is highly expressed in immune cells.Accumulating data indicated that galectin-9treatment induced T cell apoptosis and ameliorated autoimmune diseases in an exogenously modulated manner.However, endogenous role of galectin-9 in regulating T cells is largely unknown.We observed thatgalectin-9 is mostly expressed inside T cells and its membraneassociated and secreted forms are barely detected. Endogenous galectin-9 was quickly recruited to immune synapse upon T cell activation, suggesting its role in regulating TCR signaling. Our data revealed that proximal TCR signaling was impaired in galectin-9 deficient T cell, resulting in less proliferation through a Tim-3-independent pathway. Moreover, Th17 differentiation and B cell responses are downregulated in galectin-9 knockout mice. Finally, we demonstrated an inability of galectin-9 deficient T cells in the induction of T cell-transfer colitis and experimental autoimmune encephalomyelitis. Taken together, these findings indicate that intracellular galectin-9 is a positive regulator of T cell activation and modulates pathogenesis of autoimmune diseases.
Date:	2019-10
Relation:	European Journal of Immunology. 2019 Oct;49(S3):355.
Link to:	https://doi.org/10.1002/eji.201970400
JIF/Ranking 2023:	http://gateway.webofknowledge.com/gateway/Gateway.cgi?GWVersion=2&SrcAuth=NHRI&SrcApp=NHRI_IR&KeyISSN=0014-2980&DestApp=IC2JCR
Cited Times(WOS):	https://www.webofscience.com/wos/woscc/full-record/WOS:000490026901104
Appears in Collections:	[Huey-Kang Sytwu] Conference Papers/Meeting Abstract

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