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AbstractReperfusion of ischemic tissues elicits an acute inflammatory response involving serum complement, which is activated by circulating natural IgM specific to self-Ags exposed by ischemia. Recent reports demonstrating a role for the lectin pathway raise a question regarding the initial events in complement activation. To dissect the individual roles of natural IgM and lectin in activation of complement, mice bearing genetic deficiency in early complement, IgM, or mannan-binding lectin were characterized in a mesenteric model of ischemia reperfusion injury. The results reveal that IgM binds initially to ischemic Ag providing a binding site for mannan-binding lectin which subsequently leads to activation of complement and injury.

Original publication

DOI

10.4049/jimmunol.177.7.4727

Type

Journal article

Journal

The Journal of Immunology

Publisher

The American Association of Immunologists

Publication Date

01/10/2006

Volume

177

Pages

4727 - 4734