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Multiple Sclerosis: Lipids, Lymphocytes, and Vitamin D.

Colleen E Hayes1, James M Ntambi1,2

  • 1Department of Biochemistry, College of Agricultural and Life Sciences, University of Wisconsin-Madison, 433 Babcock Drive, Madison, WI 53706, USA.

Immunometabolism
|June 13, 2020
PubMed
Summary

Multiple sclerosis involves myelin damage and immune cell imbalance. Vitamin D deficiency, linked to obesity, may worsen these by affecting myelin stability and T cell regulation, suggesting interventions to combat these deficiencies could help manage MS.

Keywords:
T lymphocytesepigenetic regulationmethionine cyclemultiple sclerosismyelinnervonic acidobesityoligodendrocytesvitamin D

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Area of Science:

  • Neuroimmunology
  • Cellular Biology
  • Metabolic Disorders

Background:

  • Multiple sclerosis (MS) is characterized by central nervous system inflammation, demyelination, and remyelination failure.
  • Pathogenic CD4+ T helper 17 (Th17) cells dominate over protective CD4+ regulatory T (Treg) cells in MS.
  • Myelin integrity relies on specific lipids, and oligodendrocyte function is crucial for myelin maintenance.

Purpose of the Study:

  • To elucidate the roles of stearoyl-CoA desaturase (SCD) and nervonic acid in myelin stability.
  • To explore the impact of vitamin D deficiency on myelin pathology and Th17/Treg cell balance in MS.
  • To investigate the interplay between obesity, vitamin D, estrogen, and immune cell regulation in the context of MS.

Main Methods:

  • Review of myelin biosynthesis, structure, and function, focusing on SCD and nervonic acid.
  • Analysis of vitamin D signaling pathways involving microglia and CD4+ T cells.
  • Examination of epigenetic modifications, including DNA methylation and gene expression in T cells.
  • Discussion of the influence of obesity and hormonal factors on vitamin D status and immune responses.

Main Results:

  • Vitamin D deficiency is proposed to decrease SCD in oligodendrocytes, impairing nervonic acid synthesis and leading to myelin instability.
  • 1,25-dihydroxyvitamin D3 signaling restores Treg cell dominance by modulating the methionine cycle and epigenetic marking.
  • Vitamin D deficiency may hinder the epigenetic downregulation of specific genes (e.g., DRB1*1501) associated with MS pathogenesis.
  • Obesity exacerbates vitamin D deficiency, while estrogen and vitamin D synergize to promote Treg cell dominance in females.

Conclusions:

  • Vitamin D deficiency contributes to myelin fragmentation and Th17/Treg cell imbalance in MS through impaired nervonic acid synthesis and epigenetic dysregulation.
  • Addressing global epidemics of obesity and vitamin D deficiency may offer a therapeutic strategy to mitigate MS impact.
  • Understanding these molecular and metabolic links provides new avenues for MS research and potential interventions.