A Crucial Role for the Vitamin D Receptor in Experimental Inflammatory Bowel Diseases

  • Froicu M
  • Weaver V
  • Wynn T
 et al. 
  • 22

    Readers

    Mendeley users who have this article in their library.
  • 295

    Citations

    Citations of this article.

Abstract

The active form of vitamin D (1,25D3) suppressed the development of animal models of human autoimmune diseases including experimental inflammatory bowel disease (IBD). The vitamin D receptor (VDR) is required for all known biologic effects of vitamin D. Here we show that VDR deficiency (knockout, KO) resulted in severe inflammation of the gastrointestinal tract in two different experimental models of IBD. In the CD45RB transfer model of IBD, CD4+/CD45RBhigh T cells from VDR KO mice induced more severe colitis than wild-type CD4+/CD45RBhigh T cells. The second model of IBD used was the spontaneous colitis that develops in IL-10 KO mice. VDR/IL-10 double KO mice developed accelerated IBD and 100% mortality by 8 wk of age. At 8 wk of age, all of the VDR and IL-10 single KO mice were healthy. Rectal bleeding was observed in every VDR/IL-10 KO mouse. Splenocytes from the VDR/IL-10 double KO mice cells transferred IBD symptoms. The severe IBD in VDR/IL-10 double KO mice is a result of the immune system and not ...

Get free article suggestions today

Mendeley saves you time finding and organizing research

Sign up here
Already have an account ?Sign in

Find this document

Authors

  • Monica Froicu

  • Veronika Weaver

  • Thomas A. Wynn

  • Mary Ann McDowell

  • Jo Ellen Welsh

  • Margherita T. Cantorna

Cite this document

Choose a citation style from the tabs below

Save time finding and organizing research with Mendeley

Sign up for free