Journal
SEMINARS IN IMMUNOPATHOLOGY
Volume 34, Issue 3, Pages 415-424Publisher
SPRINGER HEIDELBERG
DOI: 10.1007/s00281-012-0307-y
Keywords
Autoimmunity; Multiple sclerosis; T cells; N-glycosylation; Mgat1; Galectin
Categories
Funding
- National Institutes of Health through National Institute of Allergy and Infectious Disease [R01AI053331, R01AI082266, F32AI081456]
- National Institutes of Health through National Heart Lung and Blood Institute [F30 HL108451]
- National Institutes of Health through Collaborative Multiple Sclerosis Research Center
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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.
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