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Blood, 1 August 2005, Vol. 106, No. 3, pp. 929-931. Prepublished online as a Blood First Edition Paper on April 21, 2005; DOI 10.1182/blood-2004-12-4955.
HEMOSTASIS, THROMBOSIS, AND VASCULAR BIOLOGY PF4/heparin complexes are T cell–dependent antigensFrom the Divisions of Hematology and Cardiology, Duke University Medical Center, Durham, NC; Department of Pediatrics, Children's Hospital of Philadelphia, PA; Department of Pathology & Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia; and Cardeza Foundation for Hematologic Research, Jefferson Medical College, Philadelphia, PA.
Heparin-induced thrombocytopenia (HIT) is a life-threatening, thrombotic disorder associated with development of anti–platelet factor 4 (anti-PF4)/heparin autoantibodies. Little is known about the antigenic and cellular requirements that initiate the immune response to these complexes. To begin to delineate mechanisms of autoantibody formation in HIT, we studied the immunizing effects of murine PF4 (mPF4)/heparin in mice with and without thymic function. Euthymic mice were injected with mPF4/heparin complexes, mPF4, heparin, or buffer. Mice injected with mPF4/heparin, but not mPF4 or heparin alone, developed heparin-dependent autoantibodies that shared serologic and functional characteristics of human HIT antibodies, including preferential binding to mPF4/heparin complexes and causing heparin- and FcR
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| Copyright © 2005 by American Society of Hematology Online ISSN: 1528-0020 | |||||||||||
IIA-dependent platelet activation. In contrast, athymic mice did not develop HIT-like antibodies. Taken together, these studies establish that PF4/heparin complexes are highly immunogenic and elicit self-reacting anti-PF4/heparin antibodies in a T cell–dependent manner. 
