| Literature DB >> 11668338 |
Y P de Jong1, A C Abadia-Molina, A R Satoskar, K Clarke, S T Rietdijk, W A Faubion, E Mizoguchi, C N Metz, M Alsahli, T ten Hove, A C Keates, J B Lubetsky, R J Farrell, P Michetti, S J van Deventer, E Lolis, J R David, A K Bhan, C Terhorst, M A Sahli.
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.Entities:
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Year: 2001 PMID： 11668338 DOI： 10.1038/ni720
Source DB: PubMed Journal: Nat Immunol ISSN： 1529-2908 Impact factor: 25.606