Core Fucosylation of the T Cell Receptor Is Required for T Cell Activation

Frontiers in Immunology

Zhi Li¹  Shanshan Mao²  Shijie Sun²  Wei Liang²  Wenzhe Li²  Tonghui Ma²  Rui Yu²  Ming Li²  Jianguo Gu³  Jianing Zhang⁴  Naoyuki Taniguchi⁵ 

[1] Clinical Laboratory, Dalian Municipal Central Hospital, Dalian, China;College of Basic Medical Sciences, Dalian Medical University, Dalian, China;Division of Regulatory Glycobiology, Institute of Molecular Biomembrane and Glycobiology, Tohoku Medical and Pharmaceutical University, Sendai, Japan;School of Life Science and Medicine, Dalian University of Technology, Panjin, China;Systems Glycobiology Research Group, Advanced Science Institute, RIKEN, Saitama, Japan;

关键词: core fucosylation;    T cell receptor;    T cell activation;    systemic lupus erythematosus;    T–B cell interaction;   

DOI  :  10.3389/fimmu.2018.00078

来源: DOAJ

【 摘 要 】

CD4+ T cell activation promotes the pathogenic process of systemic lupus erythematosus (SLE). T cell receptor (TCR) complex are highly core fucosylated glycoproteins, which play important roles in T cell activation. In this study, we found that the core fucosylation of CD4+ T cells was significantly increased in SLE patients. Loss of core fucosyltransferase (Fut8), the sole enzyme for catalyzing the core fucosylation of N-glycan, significantly reduced CD4+ T cell activation and ameliorated the experimental autoimmune encephalomyelitis-induced syndrome in Fut8−/− mice. T cell activation with OVA323–339 loaded major histocompatibility complex II (pMHC-II) on B cell was dramatically attenuated in Fut8−/−OT-II CD4+ T cells compared with Fut8+/+OT-II CD4+ T cells. Moreover, the phosphorylation of ZAP-70 was significantly reduced in Fut8+/+OT-II CD4+ T cells by the treatment of fucosidase. Our results suggest that core fucosylation is required for efficient TCR–pMHC-II contacts in CD4+ T cell activation, and hyper core fucosylation may serve as a potential novel biomarker in the sera from SLE patients.

【 授权许可】

Unknown