Development of chronic colitis is dependent on the cytokine MIF. Academic Article uri icon

Overview

abstract

  • The cytokine macrophage-migration inhibitory factor (MIF) is secreted by a number of cell types upon induction by lipopolysaccharide (LPS). Because colitis is dependent on interplay between the mucosal immune system and intestinal bacteria, we investigated the role of MIF in experimental colitis. MIF-deficient mice failed to develop disease, but reconstitution of MIF-deficient mice with wild-type innate immune cells restored colitis. In addition, established colitis could be treated with anti-MIF immunoglobulins. Thus, murine colitis is dependent on continuous MIF production by the innate immune system. Because we found increased plasma MIF concentrations in patients with Crohn's disease, these data suggested that MIF is a new target for intervention in Crohn's disease.

authors

  • de Jong, Ype P.
  • Abadia-Molina, A C
  • Satoskar, A R
  • Clarke, Kareem
  • Rietdijk, S T
  • Faubion, W A
  • Mizoguchi, Emiko
  • Metz, C N
  • Alsahli, M
  • ten Hove, Tessa
  • Keates, A C
  • Lubetsky, J B
  • Farrell, R J
  • Michetti, Pierre
  • van Deventer, S J
  • Lolis, Elias
  • David, J R
  • Bhan, A K
  • Terhorst, Cox

publication date

  • November 1, 2001

Research

keywords

  • Autoimmune Diseases
  • Colitis
  • Crohn Disease
  • Macrophage Migration-Inhibitory Factors

Identity

Scopus Document Identifier

  • 17944369782

Digital Object Identifier (DOI)

  • 10.1038/ni720

PubMed ID

  • 11668338

Additional Document Info

volume

  • 2

issue

  • 11