The Journal of Experimental Medicine
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Published online 3 January 2006 doi:10.1084/jem.20050390
Rockefeller University Press, 0022-1007 $8.00
JEM, Volume 203, Number 1, 141-152
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ARTICLE

 Identification of the target self-antigens in reperfusion injury

Ming Zhang1,2,7, Elisabeth M. Alicot7, Isaac Chiu1, Jinan Li1, Nicola Verna3, Thomas Vorup-Jensen1, Benedikt Kessler2, Motomu Shimaoka1, Rodney Chan3, Daniel Friend3, Umar Mahmood6, Ralph Weissleder6, Francis D. Moore3,5, and Michael C. Carroll1,2,4

1 CBR Institute for Biomedical Research, Inc., 2 Department of Pathology, 3 Department of Surgery, 4 Department of Pediatrics, and 5 Brigham and Women's Hospital, Harvard Medical School, Boston, MA 02115
6 Center for Molecular Imaging Research, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA 02129
7 DecImmune Therapeutics, Boston, MA 02115

CORRESPONDENCE Michael C. Carroll: carroll{at}cbr.med.harvard.edu

Reperfusion injury (RI), a potential life-threatening disorder, represents an acute inflammatory response after periods of ischemia resulting from myocardial infarction, stroke, surgery, or trauma. The recent identification of a monoclonal natural IgM that initiates RI led to the identification of nonmuscle myosin heavy chain type II A and C as the self-targets in two different tissues. These results identify a novel pathway in which the innate response to a highly conserved self-antigen expressed as a result of hypoxic stress results in tissue destruction.

Abbreviations used: ANOVA, analysis of variance; Hc, heavy chain; HRP, horseradish peroxidase; MBL, mannan-binding lectin; NMHC-II, nonmuscle myosin Hc type II; PARS, poly(ADP ribose) synthetase; PL, phospholipd; RI, reperfusion injury; ROS, reactive oxygen species; SPR, surface plasmon resonance.


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