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Interleukin‐2, Interleukin‐7, T cell‐mediated autoimmunity, and N‐glycosylation
Author(s) -
Grigorian Ani,
Mkhikian Haik,
Demetriou Michael
Publication year - 2012
Publication title -
annals of the new york academy of sciences
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.712
H-Index - 248
eISSN - 1749-6632
pISSN - 0077-8923
DOI - 10.1111/j.1749-6632.2011.06391.x
Subject(s) - autoimmunity , glycosylation , biology , glycan , immunology , immune tolerance , microbiology and biotechnology , interleukin 13 , interleukin , genetics , immune system , cytokine , glycoprotein
T cell activation and self‐tolerance are tightly regulated to provide effective host defense against foreign pathogens while deflecting inappropriate autoimmune responses. Golgi Asn (N)‐linked protein glycosylation coregulates homeostatic set points for T cell growth, differentiation, and self‐tolerance to influence risk of autoimmune disorders such as multiple sclerosis (MS). Human autoimmunity is a complex trait that develops from intricate and poorly understood interactions between an individual's genetics and their environmental exposures. Recent evidence from our group suggests that in MS, additive and/or epistatic interactions between multiple genetic and environmental risk factors combine to dysregulate a common biochemical pathway, namely Golgi N‐glycosylation. Here, we review the multiple regulatory mechanisms controlling N ‐glycan branching in T cells and autoimmunity, focusing on recent data implicating a critical role for interleukin‐2 (IL‐2) and IL‐7 signaling.