On Sep 29, 11:31=A0pm, Kofi <k...@[EMAIL PROTECTED]
> wrote:
> IL-10 is a cytokine vital to the functioning of regulatory T-cells
> (Tregs). =A0When 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. =A0Well, it turns out
> my hunch might be right. =A0CMV interferes with at least one pathway
> downstream of vitamin D3 - namely, IL-10. =A0There's precious little on
i=
t
> in the literature, though.
>
> <1> =A0An infection which improved when I quit eating turkey, by the
way.=
=A0
> IDO degrades tryptophan and has antiviral and antimicrobial properties.
=
=A0
> IDO can be blocked by surplus tryptophan - which you can find in turkey.
>
> =A0Med Hypotheses. 2008;71(1):85-90.
> =A0
> 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:
> * =A0Research Sup****t, Non-U.S. Gov't
>
> PMID: 18387750
Question: do you suppose the UV is more
effective because you get a larger dose
of vitamin D by way synthesis than the
doses you've chosen to take? Or could
it be the UV has other interactions
with your body? I am just brain storming.
I got 65 hits on Pubmed with IL-10 and
calcitriol. Not all contain relevant
information but at least some seem
on relevant. Anyway sometimes a systematic
series of searches with various search
words can reveal additional information
in my experience.
Thanks for the posting.....it was
near something I've been thinking about
a little.
Anyway it seems I'll be taking 6000 IU
of cholecalciferol per day for the Autumn and Winter months.
Understand my interest is life extension but
I know persons with some the disease processes that additional vitamin
D3 can benefit.
This looks interesting:
: Eur J Immunol. 2008 Aug;38(8):2210-8.
1,25-dihydroxyvitamin D(3) promotes IL-10 production in human B cells.
Heine G, Niesner U, Chang HD, Steinmeyer A, Z=FCgel U, Zuberbier T,
Radbruch A,
Worm M.
Allergy-Center-Charit=E9, CCM, Department of Dermatology and Allergy,
Charit=E9 -
Universit=E4tsmedizin Berlin, Berlin, Germany.
1,25-dihydroxyvitamin D(3) (calcitriol) regulates immune responses,
e.g., inhibits expression of IgE by B cells and enhances expression of
IL-10 by
dendritic cells and T cells. We re****t here that activation of human B
cells by B cell receptor, CD40 and IL-4 signals induces expression of
the gene for
25-hydroxyvitamin-D3-1alpha-hydroxylase (CYP1alpha). Accordingly,
these B cells generate and secrete significant amounts of calcitriol.
In activated B cells calcitriol induces expression of the genes Cyp24,
encoding a vitamin D hydroxylase, and Trpv6, encoding a calcium
selective channel protein. Calcitriol enhances IL-10 expression of
activated B cells more than threefold, both by recruiting the vitamin
D receptor to the promoter of Il-10, and to lesser extent by
modulation of calcium-dependent signaling. The molecular link in
activated B
cells between vitamin D signaling, expression of IgE and IL-10, and
their ability to produce calcitriol from its precursor, suggest that
pro-vitamin D
(25-hydroxyvitamin D(3)) can be used as a modulator of allergic immune
responses.
PMID: 18651709 [PubMed - indexed for MEDLINE]
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