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* Center for Experimental Therapeutics and Reperfusion Injury, Department of Noninvasive Cardiology, Brigham and Women’s Hospital, Harvard Medical School, Boston MA 02115; Laboratory of Developmental Immunology, Massachusetts General Hospital for Children, Harvard Medical School, Boston MA 02114; and Department of Discovery Research, Alexion Pharmaceuticals, Cheshire, CT 06410
The mannose-binding lectin (MBL), a circulating pattern recognition molecule, recognizes a wide range of infectious agents with resultant initiation of the complement cascade in an Ab-independent manner. MBL recognizes infectious non-self and altered self in the guise of apoptotic and necrotic cells. In this study, we demonstrate that mice lacking MBL, and hence are devoid of MBL-dependent lectin pathway activation but have fully active alternative and classical complement pathways, are protected from cardiac reperfusion injury with resultant preservation of cardiac function. Significantly, mice that lack a major component of the classical complement pathway initiation complex (C1q) but have an intact MBL complement pathway, are not protected from injury. These results suggest that the MBL-dependent pathway of complement activation is a key regulator of myocardial reperfusion ischemic injury. MBL is an example of a pattern recognition molecule that plays a dual role in modifying inflammatory responses to sterile and infectious injury.
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