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The effects of vitamin D in T helper...

The Pennsylvania State University.

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The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases.

紀錄類型:	書目-語言資料,印刷品 : Monograph/item
正題名/作者:	The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases./
作者:	Mahon, Brett D.
面頁冊數:	116 p.
附註:	Adviser: Margherita T. Cantorna.
Contained By:	Dissertation Abstracts International65-07B.
標題:	Health Sciences, Immunology. -
電子資源:	http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3140054
ISBN:	9780496871957

The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases.
Mahon, Brett D.

The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases. - 116 p.

Adviser: Margherita T. Cantorna.

Thesis (Ph.D.)--The Pennsylvania State University, 2004.

Taken together, these results help elucidate the targets of vitamin D that may play a role in ameliorating and/or preventing autoimmune diseases by regulating the Th1-driven immune response.

ISBN: 9780496871957Subjects--Topical Terms:

1017716
Health Sciences, Immunology.

The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases.
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020 $a 9780496871957
035 $a (UMI)AAI3140054
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100 1 $a Mahon, Brett D. $3 1294638
245 1 4 $a The effects of vitamin D in T helper cells and T cell mediated autoimmune diseases.
300 $a 116 p.
500 $a Adviser: Margherita T. Cantorna.
500 $a Source: Dissertation Abstracts International, Volume: 65-07, Section: B, page: 3390.
502 $a Thesis (Ph.D.)--The Pennsylvania State University, 2004.
520 $a Taken together, these results help elucidate the targets of vitamin D that may play a role in ameliorating and/or preventing autoimmune diseases by regulating the Th1-driven immune response.
520 $a Vitamin D is hypothesized to be an environmental factor important in the etiology of several T cell mediated autoimmune diseases. Vitamin D intake is inversely associated with the incidence of two human autoimmune diseases, and the active form of vitamin D [1,25dihydroxyvitaminD3 (1,25D3)] suppresses the development and severity of several animal models of autoimmune diseases. Here new data are presented concerning the ability of vitamin D and 1,25D3 to affect (1) multiple sclerosis, (2) a murine model of inflammatory bowel disease (IBD), and (3) T helper (Th) cell gene expression and cytokine production in vitro.
520 $a Multiple sclerosis patients were randomized in a double blind design, and placed into either a vitamin D supplemented group or a placebo control group. As expected, serum 25-hydroxyvitamin D levels increased significantly following 6 months of vitamin D supplementation (17 +/- 6 ng/ml at baseline vs. 28 +/- 8 ng/ml at 6 months). Vitamin D supplementation also significantly increased serum transforming growth factor (TGF)-beta1 levels from 230 +/- 21 ng/ml at baseline to 295 +/- 40 ng/ml 6 months later. Placebo treatment had no effect on serum TGF-beta1 levels. Tumor necrosis factor (TNF)-alpha, interferon (IFN)-gamma, and interleukin (IL)-13 were not different following vitamin D supplementation. IL-2 mRNA levels decreased following vitamin D supplementation but the differences did not reach significance. Vitamin D supplementation of MS patients for 6 months was associated with increased vitamin D status and serum TGF-beta1.
520 $a IL-10 KO mice represent an experimental murine model of IBD. 1,25D3 reduced the expression of LPS induced TNF-alpha associated factor (LITAF) in whole colon tissue of IL-10 KO mice. Untreated IL-10 KO mice had significantly larger small intestine to body weight ratios (9.0 +/- 0.6%) compared to 1,25D3 treated IL-10 KO mice (6.5 +/- 0.7%). IL-10 KO mice expressed higher levels of TNF-alpha in the ileum and ascending colon compared to wild type (WT) mice. The fulminating IBD that develops in VDR/IL-10 double KO mice is associated with the increased expression of TNF-alpha and LITAF. VDR/IL-10 double KO mice express significantly more TNF-alpha and LITAF than either single KO strain. 1,25D3 intake was inversely associated with IBD severity, and corresponded with the reduced expression of LITAF in colonic tissue of IL-10 KO mice.
520 $a In vitro 1,25D3 treatment decreased the proliferation of all Th cells and decreased the production of IFN-gamma, IL-2, and IL-5. In Th2 cells, 1,25D3 increased the production of IL-4. Quiescent CD4+ T cells express vitamin D receptors but only at a low level which increased 5-fold following 24 hr activation. 1,25D3 treatment of Th0 cells, but not Th1 or Th2 cells, induced the expression of the transcription factor GATA-3. Microarray technology identified over one hundred targets of 1,25D3 in CD4+ T cells. Of interest were 2 genes involved in NF-kappaB regulation, the IL-2Rbeta gene and IgE binding factor. Th2 and Th0 cells produced more IgE binding factor after treatment with 1,25D3 while Th1 cell IgE binding factor expression was unaffected by 1,25D3 addition. 1,25D3 is a direct regulator of Th cell effector function and Th cell development. The targets of 1,25D3 in CD4+ T cells depend on the activation and differentiation status of the T cells.
590 $a School code: 0176.
650 4 $a Health Sciences, Immunology. $3 1017716
650 4 $a Health Sciences, Nutrition. $3 1017801
690 $a 0570
690 $a 0982
710 2 0 $a The Pennsylvania State University. $3 699896
773 0 $t Dissertation Abstracts International $g 65-07B.
790 $a 0176
790 1 0 $a Cantorna, Margherita T., $e advisor
791 $a Ph.D.
792 $a 2004
856 4 0 $u http://pqdd.sinica.edu.tw/twdaoapp/servlet/advanced?query=3140054