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    Nat Immunol. 2001 Nov;2(11):1061-6.

    Development of chronic colitis is dependent on the cytokine MIF.

    de Jong YP, Abadia-Molina AC, Satoskar AR, Clarke K, Rietdijk ST, Faubion WA, Mizoguchi E, Metz CN, Alsahli M, ten Hove T, Keates AC, Lubetsky JB, Farrell RJ, Michetti P, van Deventer SJ, Lolis E, David JR, Bhan AK, Terhorst C.

    Source

    Division of Immunology, Beth Israel Deaconess Medical Center, Boston, MA 02215, USA.

    Erratum in

    • Nat Immunol 2002 Apr;3(4):407. Sahli MA [corrected to Alsahli M].

    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.

    PMID:
    11668338
    [PubMed - indexed for MEDLINE]

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