all things vitamin D

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Postby CVfactor » Mon May 23, 2011 4:20 pm

The article in the previous posts explains a lot about T-Cells and I think I will summarize it as follows:

1. It appears that MS is a T-cell mediated disease. In particular, helper T-cells otherwise known as Th cells (specifically the pro inflamitory helper T-cells Th1 and Th17).

2. Helper T-cells do not directly interact with tissues, but they recruit other cells such as macrophages and neutrophils to perform the actual cell destruction found in MS lesions via cytokines (chemical signals).

This is why T-cells are found surrounding the lesion at its surface but are rarely found within the lesion (in contrasts macrophages and neutrophils are found in the lesion).

3. It appears that helper t-cells are self reactive when they are developed in the thymus because they are not exposed to all auto-antigens during development. This is true of healthy individuals also.

4. It is the job of regulatory T-cells (Tregs) to prevent these helper T-cells from initiating a response against tissues in the central nervous system.

5. It seems that regulatory T-cells in people with MS are defective in providing this protection.

Here is another article that explains this in more detail:

http://www.sciencedirect.com/science/ar ... 1410000043

6. It seems that there is another variant of regulatory T-cells that can be developed that are separate from the naturally occurring regulatory T-cells which can prevent an auto-immune response by helper T-cells. These are known as induced or adaptive regulatory T-cells (iTreg, aTreg).

7. There is mounting evidence that Vitamin D (a steroid hormone) appears to promote the development of regulatory T-cell function.
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Vitamin D levels low in African-Americans with MS

Postby MSUK » Mon May 23, 2011 10:55 pm

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African-Americans who have multiple sclerosis (MS) have lower vitamin D levels than African-Americans who don't have the disease, according to a study published in the May 24, 2011, print issue of Neurology®, the medical journal of the American Academy of Neurology. However, most of the difference in vitamin D levels was due to differences in climate and geography.

"MS is not as common in African-Americans as it is in whites, although the disease tends to be more severe in African-Americans," said study author Ari J. Green, MD, of the University of California San Francisco and a member of the American Academy of Neurology. "We have known that vitamin D levels are associated with MS and that African-Americans are at increased risk for having low vitamin D levels, but little research has been done to look at vitamin D levels in African-Americans with MS."... Read More - http://www.msrc.co.uk/index.cfm/fuseact ... ageid/1334
MS-UK - http://www.ms-uk.org/
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Postby CVfactor » Mon Jun 06, 2011 2:55 pm

It appears that there is a lot of research now being conducted on regulatory T cells in areas where self tolerance is defficient (autoimmune diseases and allergy) as well as when tolerance needs to be induced (transplant rejection).

Here is a recent Podcast with Professor Robert Lechler, King's College London who is working on regulatory T-cells therapies to prevent transplant rejection, but also describes how these cells are crucial in the prevention of autoimmune diseases such as MS and Rheumatoid Arthritis:

http://nakeddiscovery.com/downloads/split_individual/11.05.22/Naked_Scientists_Show_11.05.22_8516.mp3
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Postby CVfactor » Wed Jun 22, 2011 5:01 pm

Here is an article that was published in Scientific America about regulatory T-cells. It describes how they are believed to control many different autoimmune diseases:

http://www.smccd.net/accounts/digennaroc/biology430/Articles/Regulatory_T-cells.pdf
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Postby CVfactor » Thu Jun 23, 2011 5:01 pm

Here is a review article about regulatory T-cells and their function in autoimune diseases from The New England Journal of Medicine:

http://www.oncoinmun.cl/pdf2008/ihq2008/1166.pdf
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Postby CVfactor » Sun Jun 26, 2011 3:02 pm

As shown in this thread, many researchers investigating autoimmune diseases are finding that the Treg function of people with these diseases are defective.

Here is another paper by researchers investigating chronic inflammatory demyelinating polyradiculoneuropathy (CIDP) which is a disease similar to MS that effects the meylin sheath in the periphery (not the CNS).

http://www.ncbi.nlm.nih.gov/pubmed/19886739

Conclusion is that Tregs are defective in people with CIDP compared with healthy controls.
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Postby CVfactor » Tue Jul 05, 2011 4:46 pm

To explain a little more about vitamin D and its connection to regulatory T cells, I would first like to summarize some facts about Vitamin D.

1. Vitamin D is not a vitamin. It is a steroid hormone. You cannot get natural amounts of vitamin D from foods. For example, a healthy person in mid-day summer sun can synthesis 10,000 IU's of vitamin D in 1 hour. Compare this to the amount that is fortified in a glass of milk which is about 200 IU's.

2. There are three stages to vitamin D synthesis in the body. The first is called Cholecalciferol which is generated by UV exposure. This is the same as Vitamin D3 that you can purchase at any drug store.

Cholecalciferol is then hydroxylated in the liver to become calcifediol (25-hydroxyvitamin D3, otherwise known as Calcidiol). This is the main circulating form in your blood and is what should be checked by your doctor.

Finally, calcifediol is again hydroxylated, this time in the kidney but also by immune cells, and becomes calcitriol (1,25-dihydroxyvitamin D3). Calcitriol is the most active hormone form of vitamin D3.


3. There is mounting evidence that Vitamin D3 has a direct effect on regulatory T-cells. These Treg-cells restrain the immune system to prevent autoimune diseases and maintain self tolerance.

It appears from the mounting evidence that Tregs are defective in their supressive function in people with MS as well as other autoimune diseases.

I believe this is why there is such great success with the HSCT procedure, because it wipes out these defective Tregs and enables normal Tregs to perform their proper function in people with auto-immune diseases.

The key thing to remember is that all people generate self-reactive immune cells, but it appears that people with autoimmune diseases lack the function to shut-down an autoimmune response because of the lack of suppressing ability of their Tregs.

Here is a recent article that describes this:

http://www.ima.org.il/imaj/ar10mar-11.pdf

So to me, it is a no brainer to follow the recent studies of high doses of vitamin D (Phase I/II) on people with MS. I cannot understand why the MS community is not pushing for more research on vitamin D to find the optimum levels. There has been suspicion of a connection of vitamin D's role in preventing MS for more than 30 years, but little has been done to investigate this.
Last edited by CVfactor on Mon Jul 11, 2011 2:29 pm, edited 1 time in total.
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Re: Vitamin D3

Postby NHE » Wed Jul 06, 2011 12:36 am

Here's some more info on Vitamin D3.

Relapse frequency has been found to correlate inversely with vitamin D3 levels. 50-60 ng/mL (125-150 nmol/L) is a good target range. Note, the conversion factor for 25(OH) vitamin D3 ng/mL -> nmol/L = 2.496

post128403.html#p128403

higher 25-OH-D levels were associated with a reduced hazard of relapse. This occurred in a dose-dependent linear fashion, with each 10nmol/l increase in 25-OH-D resulting in up to a 12% reduction in risk of relapse. Clinically, raising 25-OH-D levels by 50nmol/l could halve the hazard of a relapse.


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Postby jimmylegs » Wed Jul 06, 2011 3:20 pm

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Postby CVfactor » Wed Jul 06, 2011 4:42 pm

I don't know why there is such an unwillingness to investigate vitamin D. It seems that the only work being done is by NIH grants on the basic science and a few initial trials from researchers outside of the U.S.

I think the National MS Society has really dropped the ball here. When I first got sick and found out that MS has a latitude gradient and this may be due to sunlight exposure and vitamin D levels, I had to ask myself why isn't this being researched more fully?

It would be a shame if the cure for MS (and many other autoimune diseases) is simply a matter of having the right level of serum 25OHD3. Something that could be taken care of from supplementation that is readily available at any drug store.

Personally, I think there is a revolution waiting to happen in healthcare and Vitamin D is the key.

Here is a good organization that also feels the same way:

http://www.vitamindcouncil.org/
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Postby CVfactor » Fri Jul 08, 2011 4:15 pm

Continuing on with the theory that regulatory Tcells (Tregs) provide a protective role against self reactive immune cells in many types of diseases here is a very recent paper that describes the state of Tregs in ALS or more commonly known as Lou Gehrig's disease.

http://brain.oxfordjournals.org/content/134/5/1293.abstract

"These observations were extended into the amyotrophic lateral sclerosis patient population where patients with more rapidly progressing disease had decreased numbers of regulatory T lymphocytes; the numbers of regulatory T lymphocytes were inversely correlated with disease progression rates. These data suggest a cellular mechanism whereby endogenous regulatory T lymphocytes are immunocompetent and actively contribute to neuroprotection through their interactions with microglia. Furthermore, these data suggest that immunotherapeutic interventions must begin early in the pathogenic process since immune dysfunction occurs at later stages."

So, it appears that Treg dysfunction and/or population reduction is key to many diseases outside of MS.
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Postby CVfactor » Sat Jul 09, 2011 4:05 pm

More information about regulatory T-cells as modulators of diseases besides MS, here is a paper that investigates Treg function in a mouse model of HIV-1 Enchephalitis:

http://www.ncbi.nlm.nih.gov/pubmed/20846730

Treg readily migrated across the blood brain barrier and were retained within virus-induced neuroinflammatory sites. In non-inflamed peripheral tissues (liver and spleen) Treg were depleted. These observations demonstrate that Treg migrate to sites of inflammation where they modulate immune responses.


In my view it appears the key is not the fact that immune cells target the bodies own tissue, it is the fact that the regulatory T cells (Tregs) are failing to shut-down the attack on the self.
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Postby CVfactor » Mon Jul 11, 2011 2:22 pm

It looks like there is a revolution happening in health science at this moment with the discovery of regulatory T-cells and diseases and self tolerance.

Here is a good video discussion Tregs and their application in transplant rejection as well as their role in autoimune diseases.

http://www.youtube.com/watch?v=PYHvVj2qaDE

And here is a video discussion regarding Tregs and Parkinsons disease:

http://www.youtube.com/watch?v=2ZJL5pAGTZo

It looks like Tregs will be the basis for future therapies in preventing many types of disease as well as transplant rejection.
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Postby CVfactor » Tue Jul 12, 2011 4:33 pm

Here is a new paper on vitamin D and MS:

http://www.ncbi.nlm.nih.gov/pubmed/21723567

Abstract
Although Vitamin D is best known as a modulator of calcium homeostasis, it also has immune modulating potential. A protective effect of Vitamin D on Multiple Sclerosis (MS) is supported by the reduced risk associated with sun exposure and use of Vitamin D supplements. Moreover, high circulating levels of Vitamin D have been associated with lower risk of MS. To gain more insight into putative regulatory mechanisms of Vitamin D in MS pathogenesis, we studied 132 Hispanic patients with clinically definite MS, 58 with relapsing remitting MS (RR MS) during remission, 34 RR MS patients during relapse, and 40 primary progressive MS cases (PP MS). Sixty healthy individuals matched with respect to place of residence, race/ethnicity, age and gender served as controls. Levels of 25(OH) Vitamin D and 1,25(OH)(2) Vitamin D, measured by ELISA were significantly lower in RR MS patients than in controls. In addition, levels in patients suffering relapses were lower than during remissions. By contrast, PP MS patients showed similar values to controls. Proliferation of both freshly isolated CD4+ T cells and MBP-specific T cells was significantly inhibited by 1,25(OH)(2) Vitamin D. Moreover, activated Vitamin D enhanced the development of IL-10 producing cells, and reduced the number of IL-6 and IL-17 secreting cells. Notably, VDR expression was induced by 1,25(OH)(2) Vitamin D in both activated and resting cells. Interestingly, T cells were able to metabolize 25(OH) Vitamin D into biologically active 1,25(OH)(2) Vitamin D, since T cells express 1α-hydroxylase constitutively. Finally, 1,25(OH)(2) Vitamin D also increased the expression and biological activity of IDO, triggering significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these findings suggest that 1,25(OH)(2) VitaminD plays an important role in T cell homeostasis during the course of MS, suggesting correction of its deficiency may be useful during treatment of the disease.


And again, more evidence that Vitamin D promotes Treg cell function/population.
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Re: Vitamin D

Postby NHE » Wed Jul 13, 2011 1:12 am

CVfactor wrote:Here is a new paper on vitamin D and MS:

http://www.ncbi.nlm.nih.gov/pubmed/21723567

...T cells were able to metabolize 25(OH) Vitamin D into biologically active 1,25(OH)(2) Vitamin D, since T cells express 1α-hydroxylase constitutively. Finally, 1,25(OH)(2) Vitamin D also increased the expression and biological activity of IDO, triggering significant increase in the number of CD4+CD25+ T regulatory cells. Collectively, these findings suggest that 1,25(OH)(2) VitaminD plays an important role in T cell homeostasis during the course of MS, suggesting correction of its deficiency may be useful during treatment of the disease.


And again, more evidence that Vitamin D promotes Treg cell function/population.


Here's a good review paper on vitamin D. The full paper is free. It discusses many aspects of the activity of vitamin D so don't be dissuaded by the abstract.

http://www.ncbi.nlm.nih.gov/pubmed/15951480


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