IL-10 is a cytokine vital to the functioning of regulatory T-cells
(Tregs). When I found out I had a raging CMV infection<1>, I ran a
literature search cross-referencing members of the herpesvirus family
with vitamin D3 to see if I could explain why oral supplementation with
D3 is much less effective for me than UV exposure. Well, it turns out
my hunch might be right. CMV interferes with at least one pathway
downstream of vitamin D3 - namely, IL-10. There's precious little on it
in the literature, though.
<1> An infection which improved when I quit eating turkey, by the way.
IDO degrades tryptophan and has antiviral and antimicrobial properties.
IDO can be blocked by surplus tryptophan - which you can find in turkey.
Med Hypotheses. 2008;71(1):85-90.
A unifying multiple sclerosis etiology linking virus infection,
sunlight, and vitamin D, through viral interleukin-10.
Hayes CE, Donald Acheson E.
Department of Biochemistry, University of Wisconsin, Madison, 433
Babcock Drive, Madison, WI 53706, USA.
Multiple sclerosis (MS) is a neurodegenerative disease of uncertain
etiology. In MS, neurodegeneration is thought to be secondary to
autoimmune-mediated damage. However, no cohesive explanation yet exists
as to how environmental factors interact to induce a neurodegenerative
autoimmune response. Insufficient sunlight exposure and chronic viral
infections have been proposed as unrelated environmental risk factors
for MS. We suggest that these risk factors may act synergistically to
enable the pathogenic autoimmune response. Low ultraviolet light (UVL)
exposure depletes vitamin D3 stores, and low vitamin D3 levels correlate
strongly with high MS risk. The central nervous system converts vitamin
D3 into 1,25-dihydroxyvitamin D3 (1,25-(OH)2 D3), a biologically active
hormone with anti-inflammatory and neuro-protective functions that
depend on IL-10-producing regulatory lymphocytes. Herpesvirus infection
also correlates with MS risk. Some herpesviruses like Epstein-Barr virus
produce an IL-10-like cytokine termed vIL-10. We hypothesize that vIL-10
may induce a dysfunction of IL-10-producing regulatory lymphocytes,
thereby undermining the protective functions of sunlight, vitamin D3,
and 1,25-(OH)2 D3. The vIL-10 could elicit a host immune response
capable of neutralizing or depleting IL-10, or the vIL-10 could compete
with IL-10 but fail to perform an essential IL-10 function. In either
case, the lack of sunlight exposure and the herpes virus infection might
synergize to induce a defect in IL-10-producing regulatory lymphocyte
function that undermines self-tolerance mechanisms and enables a
pathogenic autoimmune response to neural proteins.
Publication Types:
* Research Sup****t, Non-U.S. Gov't
PMID: 18387750
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