Development of experimental autoimmune encephalomyelitis (EAE) in mice requires vitamin D and the vitamin D receptor

被引：47

作者：

Wang, Yanping ^{[1
]}

Marling, Steven J. ^{[1
]}

Zhu, Jinge G. ^{[1
]}

Severson, Kyle S. ^{[1
]}

DeLuca, Hector F. ^{[1
]}

机构：

[1] Univ Wisconsin, Dept Biochem, Madison, WI 53706 USA

来源：

PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA | 2012年 / 109卷 / 22期

关键词：

autoimmune disease; serum calcium; serum 25-hydroxyvitamin D3; CYP27B1 knockout mice; CYP2R1 knockout mice; MULTIPLE-SCLEROSIS; 1,25-DIHYDROXYVITAMIN D-3; 1,25-DIHYDROXYCHOLECALCIFEROL; PREVALENCE; SEVERITY; RISK;

D O I：

10.1073/pnas.1206054109

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

The development of experimental autoimmune encephalomyelitis (EAE), a model of multiple sclerosis, has been studied in mice that were (i) vitamin D-deficient, (ii) minus the vitamin D receptor, (iii) minus a vitamin D 25-hydroxylase, and (iv) minus the vitamin D 25-hydroxyvitamin D-1 alpha-hydroxylase. EAE development was markedly suppressed in mice lacking the vitamin D receptor and partially suppressed in vitamin D-insufficient mice. However, the absence of either of the two key hydroxylases (i. e., 25-hydroxylase and 1 alpha-hydroxylase) neither inhibits nor enhances the development of EAE. These results indicate that vitamin D and the vitamin D receptor are required for the development of EAE. The results also suggest that 1,25-dihydroxyvitamin D3 may not play a role in this autoimmune response.

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页码：8501 / 8504

页数：4

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