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论文类型：期刊论文

发表时间：2018-01-29

发表刊物：FRONTIERS IN IMMUNOLOGY

收录刊物：SCIE、PubMed、Scopus

卷号：9

期号：JAN

页面范围：78

ISSN号：1664-3224

关键字：core fucosylation; T cell receptor; T cell activation; systemic lupus erythematosus; T-B cell interaction

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.