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From the Department of Immunology, Rush Medical College, and the Department of Microbiology, University of Illinois at the Medical Center, Chicago, Illinois 60612
Abstract
C-reactive protein (CRP) is an acute phase reactant which shares numerous functional characteristics with the immunoglobulins. In the present study CRP was found to inhibit the aggregation of human platelets stimulated by either modified human immunoglobulin or thrombin. This effect did not involve chelation of calcium or cytotoxicity, and was overcome by larger amounts of the aggregating agents. CRP also inhibited the activation but not the activity of platelet factor 3 and the release of
-glucuronidase. Thus, CRP can inhibit multiple platelet reactivities. We suggest that this property of CRP may play an important role in the control of platelet responsiveness during reactions of inflammation, defense, and repair.
Footnotes
1 This work was supported by Grant AI 12870-01 from the National Institutes of Health, and by grants from the Chicago Heart Association, Leukemia Research Foundation, Inc., and Hunter Trust.
2 This work was presented in part to the American Society for Experimental Pathology April 16, 1975 (1).
3 H. G. holds the Thomas J. Coogan, Sr., Chair of Immunology established by Marjorie Lindheimer Everett.
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