Journal
NATURE IMMUNOLOGY
Volume 2, Issue 11, Pages 1061-1066Publisher
NATURE AMERICA INC
DOI: 10.1038/ni720
Keywords
-
Categories
Funding
- NIAID NIH HHS [AI25532] Funding Source: Medline
- NIDDK NIH HHS [DK52510, DK47677, DK43351] Funding Source: Medline
Ask authors/readers for more resources
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
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available