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Ann N Y Acad Sci. 2012 Apr;1253:49-57. doi: 10.1111/j.1749-6632.2011.06391.x. Epub 2012 Jan 30.

Interleukin-2, Interleukin-7, T cell-mediated autoimmunity, and N-glycosylation.

Author information

1
Department of Neurology, University of California, Irvine, USA.

Abstract

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.

PMID:
22288682
PMCID:
PMC4520414
DOI:
10.1111/j.1749-6632.2011.06391.x
[Indexed for MEDLINE]
Free PMC Article

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