The modulatory roles of T cell glycosylation in systemic lupus erythematosus.

Affiliation

Long Y(1), Hu C(1), Zeng X(2).
Author information:
(1)Department of Rheumatology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, National Clinical Research Center for Dermatologic and Immunologic Diseases, Ministry of Science and Technology, Beijing, China.
(2)Department of Rheumatology, Peking Union Medical College Hospital, Peking Union Medical College and Chinese Academy of Medical Sciences, Key Laboratory of Rheumatology and Clinical Immunology, Ministry of Education, National Clinical Research Center for Dermatologic and Immunologic Diseases, Ministry of Science and Technology, Beijing, China. [Email]

Abstract

Systemic lupus erythematosus (SLE) is a complex and challenging disorder. At present, abnormal T cells are considered to be the key point in the pathogenesis of SLE, including the losing central immune tolerance of self-reactive T cells in the thymus, breaking of regulatory T cell balances, and the overactivation of pro-inflammatory T cells. The alterations of T-cell receptor proteins are closely related to these abnormal changes. Glycosylation is one of the most ubiquitous steps of protein post-translational modification. Especially the modifications of N-glycans and O-glycans on T-cell surfaces have been found to regulate apoptosis and downstream signalling in SLE. Accordingly, this review summarises the aberrant modulate effects of T cell glycosylation in SLE and provides new insights into understanding the pathogenesis and some potential therapeutic targets of this chronic autoimmune disease.