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Pathogenesis of multiple sclerosis via environmental and genetic dysregulation of N-glycosylation.


ABSTRACT: Autoimmune diseases such as multiple sclerosis (MS) result from complex and poorly understood interactions of genetic and environmental factors. A central role for T cells in MS is supported by mouse models, association of the major histocompatibility complex region, and association of critical T cell growth regulator genes such as interleukin-2 receptor (IL-2RA) and interleukin-7 receptor (IL-7RA). Multiple environmental factors (vitamin D(3) deficiency and metabolism) converge with multiple genetic variants (IL-7RA, IL-2RA, MGAT1, and CTLA-4) to dysregulate Golgi N-glycosylation in MS, resulting in T cell hyperactivity, loss of self-tolerance and in mice, a spontaneous MS-like disease with neurodegeneration. Here, we review the genetic and biological interactions that regulate MS pathogenesis through dysregulation of N-glycosylation and how this may enable individualized therapeutic approaches.

SUBMITTER: Grigorian A 

PROVIDER: S-EPMC3960996 | biostudies-literature | 2012 May

REPOSITORIES: biostudies-literature

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Pathogenesis of multiple sclerosis via environmental and genetic dysregulation of N-glycosylation.

Grigorian Ani A   Mkhikian Haik H   Li Carey F CF   Newton Barbara L BL   Zhou Raymond W RW   Demetriou Michael M  

Seminars in immunopathology 20120411 3


Autoimmune diseases such as multiple sclerosis (MS) result from complex and poorly understood interactions of genetic and environmental factors. A central role for T cells in MS is supported by mouse models, association of the major histocompatibility complex region, and association of critical T cell growth regulator genes such as interleukin-2 receptor (IL-2RA) and interleukin-7 receptor (IL-7RA). Multiple environmental factors (vitamin D(3) deficiency and metabolism) converge with multiple ge  ...[more]

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