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1,25-Dihydroxyvitamin D3 inhibits the differentiation and migration of T(H)17 cells to protect against experimental autoimmune encephalomyelitis

Authors
 Jae-Hoon Chang  ;  Hye-Ran Cha  ;  Dong-Sup Lee  ;  Kyoung Yul Seo  ;  Mi-Na Kweon 
Citation
 PLOS ONE, Vol.5(9) : e12925, 2010 
Journal Title
 PLOS ONE 
Issue Date
2010
MeSH
Animals ; Calcitriol/administration & dosage* ; Cell Differentiation/drug effects* ; Cell Movement/drug effects ; Down-Regulation* ; Encephalomyelitis, Autoimmune, Experimental/drug therapy* ; Encephalomyelitis, Autoimmune, Experimental/immunology ; Encephalomyelitis, Autoimmune, Experimental/physiopathology ; Encephalomyelitis, Autoimmune, Experimental/prevention & control ; Female ; Humans ; Interleukin-2/immunology ; Mice ; Mice, Inbred BALB C ; Mice, Inbred C57BL ; Mice, Knockout ; Multiple Sclerosis/drug therapy* ; Multiple Sclerosis/immunology ; Multiple Sclerosis/physiopathology ; Multiple Sclerosis/prevention & control ; Protective Agents/administration & dosage* ; Th17 Cells/cytology* ; Th17 Cells/drug effects ; Th17 Cells/immunology
Abstract
BACKGROUND: Vitamin D(3), the most physiologically relevant form of vitamin D, is an essential organic compound that has been shown to have a crucial effect on the immune responses. Vitamin D(3) ameliorates the onset of the experimental autoimmune encephalomyelitis (EAE); however, the direct effect of vitamin D(3) on T cells is largely unknown. METHODOLOGY/PRINCIPAL FINDINGS: In an in vitro system using cells from mice, the active form of vitamin D(3) (1,25-dihydroxyvitamin D(3)) suppresses both interleukin (IL)-17-producing T cells (T(H)17) and regulatory T cells (Treg) differentiation via a vitamin D receptor signal. The ability of 1,25-dihydroxyvitamin D(3) (1,25(OH)(2)D(3)) to reduce the amount of IL-2 regulates the generation of Treg cells, but not T(H)17 cells. Under T(H)17-polarizing conditions, 1,25(OH)(2)D(3) helps to increase the numbers of IL-10-producing T cells, but 1,25(OH)(2)D(3)'s negative regulation of T(H)17 development is still defined in the IL-10(-/-) T cells. Although the STAT1 signal reciprocally affects the secretion of IL-10 and IL-17, 1,25(OH)(2)D(3) inhibits IL-17 production in STAT1(-/-) T cells. Most interestingly, 1,25(OH)(2)D(3) negatively regulates CCR6 expression which might be essential for T(H)17 cells to enter the central nervous system and initiate EAE. CONCLUSIONS/SIGNIFICANCE: Our present results in an experimental murine model suggest that 1,25(OH)(2)D(3) can directly regulate T cell differentiation and could be applied in preventive and therapeutic strategies for T(H)17-mediated autoimmune diseases.
Files in This Item:
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DOI
10.1371/journal.pone.0012925
Appears in Collections:
1. College of Medicine (의과대학) > Dept. of Ophthalmology (안과학교실) > 1. Journal Papers
Yonsei Authors
Seo, Kyuong Yul(서경률) ORCID logo https://orcid.org/0000-0002-9855-1980
URI
https://ir.ymlib.yonsei.ac.kr/handle/22282913/101868
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