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,¶,**
,¶,
* CBR Institute of Biomedical Research,
Department of Pathology,
Department of Pediatrics, and
Department of Surgery, Harvard Medical School, Boston, MA 02115;
¶ Massachusetts General Hospital, Boston, MA 02114;
|| Brigham and Women’s Hospital, Boston, MA 02115;
# DecImmune Therapeutics, Boston, MA 02115; and
** Department of Medical Microbiology and Immunology, University of Aarhus, Aarhus, Denmark
Reperfusion 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.
The costs of publication of this article were defrayed in part by the payment of page charges. This article must therefore be hereby marked advertisement in accordance with 18 U.S.C. Section 1734 solely to indicate this fact.
1 This study was supported by National Institutes of Health Grant P50 GM52585 (to M.C.C. and F.D.M.).
2 Current address: Department of Anesthesiology, State University of New York-Downstate Medical Center, 450 Clarkson Avenue, Brooklyn, NY 11203.
3 Address correspondence and reprint requests to Michael C. Carroll, CBR Institute for Biomedical Research, Inc., Harvard Medical School, 800 Huntington Avenue, Boston, MA 02115. E-mail address: carroll{at}cbrinstitute.org
4 Abbreviations used in this paper: I/R, ischemia/reperfusion; WT, wild type; NMHC-II, nonmuscle myosin H chain type II; MASP, MBL-associated serine protease; Tw, Tween 20.
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