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Antibodies recognizing complexes of the chemokine platelet factor 4(PF4-CXCL4) and polyanions (P) opsonize PF4-coated bacteria hereby mediatingbacterial host defense. A subset of these antibodies may activate plateletsafter binding to PF4-heparin complexes, causing the prothrombotic adverse drugreaction heparin-induced thrombocytopenia (HIT). In autoimmune-HIT,anti-PF4-P-antibodies activate platelets in the absence of heparin. Here weshow that antibodies with binding forces of approximately 60-100 pN activateplatelets in the presence of polyanions, while a subset of antibodies fromautoimmune-HIT patients with binding forces greater than 100 pN binds to PF4alone in the absence of polyanions. These antibodies with high binding forcescluster PF4-molecules forming antigenic complexes which allow binding ofpolyanion-dependent anti-PF4-P-antibodies. The resulting immunocomplexes inducemassive platelet activation in the absence of heparin. Antibody-mediatedchanges in endogenous proteins that trigger binding of otherwise non-pathogenic(or cofactor-dependent) antibodies may also be relevant in otherantibody-mediated autoimmune disorders.

Anti-platelet factor 4/polyanion antibodies mediate a new mechanism of autoimmunity