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Int. J. Mol. Sci. 2018, 19(3), 780; https://doi.org/10.3390/ijms19030780

The Modulatory Roles of N-glycans in T-Cell-Mediated Autoimmune Diseases

1
Department of Microbiology and Immunology, National Defense Medical Center, No.161, Section 6, Min Chuan East Road, Neihu, Taipei 114, Taiwan
2
Graduate Institute of Life Sciences, National Defense Medical Center, No. 161, Section 6, Min Chuan East Road, Neihu, Taipei 114, Taiwan
3
Molecular Cell Biology, Taiwan International Graduate Program, Academia Sinica, Taipei 115, Taiwan
*
Author to whom correspondence should be addressed.
Received: 31 January 2018 / Revised: 28 February 2018 / Accepted: 6 March 2018 / Published: 8 March 2018
(This article belongs to the Special Issue Glycosylation and Glycoproteins 2017)
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Abstract

Glycosylation is a ubiquitous posttranslational modification of proteins that occurs in the endoplasmic reticulum/Golgi. N-glycans and mucin-type O-glycans are achieved via a series of glycohydrolase- and glycosyltransferase-mediated reactions. Glycosylation modulates immune responses by regulating thymocyte development and T helper cell differentiation. Autoimmune diseases result from an abnormal immune response by self-antigens and subsequently lead to the destruction of the target tissues. The modification of N-glycans has been studied in several animal models of T-cell-mediated autoimmune diseases. This review summarizes and highlights the modulatory effects of N-glycosylation in several autoimmune diseases, including multiple sclerosis, systemic lupus erythematosus, inflammatory bowel disease, and type 1 diabetes mellitus. View Full-Text
Keywords: N-glycan; O-glycan; autoimmune disease; multiple sclerosis; inflammatory bowel disease systemic lupus erythematosus; type 1 diabetes mellitus N-glycan; O-glycan; autoimmune disease; multiple sclerosis; inflammatory bowel disease systemic lupus erythematosus; type 1 diabetes mellitus
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Chien, M.-W.; Fu, S.-H.; Hsu, C.-Y.; Liu, Y.-W.; Sytwu, H.-K. The Modulatory Roles of N-glycans in T-Cell-Mediated Autoimmune Diseases. Int. J. Mol. Sci. 2018, 19, 780.

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