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Published on: December 9, 2015
Vitamin D status modulates the immune response to Epstein Barr virus: Synergistic effect of risk factors in multiple
1Institute of Immunology, University of Oslo, Rikshospitalet-Radiumhospitalet Medical Center and Department of Neurology, Ulleval University Hospital, 0027 Oslo, Norway. trygve.holmoy@medisin.uio.no
Abstract:
MS risk is associated with low vitamin D status prior to disease, and Epstein Barr virus (EBV) infection seems to be a prerequisite for MS. EBV could activate autoreactive T cells by several mechanisms, but it is not clear why this leads to MS. Only a small proportion of those infected with EBV develops MS, whereas autoreactive T cells are present in the normal T cell repertoire. Genetic factors cannot explain this enigma alone, because the genetic predisposition to MS in most cases is quite weak. Vitamin D receptors are expressed on EBV infected B cells, antigen presenting cells and activated lymphocytes, and the bioactive vitamin D metabolite dihydroxyvitamin D(3) suppresses antibody production and T cell proliferation and skews T cells towards a less detrimental Th2 phenotype. EBV infected B cells constitute a constant challenge to the immune system, also during seasonal periods of relative low vitamin D status. I propose that vitamin D modulates the immune response to EBV, and that detrimental activation of autoreactive T cells leading to MS is more likely if the vitamin D status is suboptimal.
Insights
Low vitamin D levels may increase multiple sclerosis (MS) risk by affecting the immune response to Epstein-Barr virus (EBV). Suboptimal vitamin D status could promote the detrimental activation of autoreactive T cells, leading to MS development.
Area of Science:
- Immunology
- Neuroscience
- Endocrinology
Background:
- Multiple Sclerosis (MS) risk is linked to low vitamin D status preceding disease onset.
- Epstein-Barr virus (EBV) infection is considered a prerequisite for MS development.
- The precise mechanism by which EBV triggers MS in a subset of infected individuals remains unclear.
Purpose of the Study:
- To investigate the role of vitamin D in modulating the immune response to EBV.
- To explore the hypothesis that suboptimal vitamin D status increases the likelihood of MS development following EBV infection.
Main Methods:
- Review of existing literature on vitamin D, EBV, and MS.
- Analysis of vitamin D receptor expression on immune cells involved in EBV infection.
- Examination of vitamin D's known immunomodulatory effects on T cell proliferation and phenotype.
Main Results:
- Vitamin D receptors are present on EBV-infected B cells, antigen-presenting cells, and activated lymphocytes.
- The active metabolite of vitamin D, dihydroxyvitamin D(3), suppresses antibody production and T cell proliferation.
- Vitamin D influences T cell differentiation towards a less detrimental Th2 phenotype.
Conclusions:
- Vitamin D plays a crucial role in modulating the immune system's response to EBV.
- Suboptimal vitamin D levels may enhance the risk of developing MS by promoting autoreactive T cell activation.
- Maintaining adequate vitamin D status could be a potential strategy to mitigate MS risk in EBV-infected individuals.
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