
<ArticleTitle>Antibodies from patients with heparin-induced thrombocytopenia stimulate monocytic cells to express tissue factor and secrete <prot>interleukin-8</prot>.</ArticleTitle>
<AbstractText>Thrombosis is a life-threatening complication that occurs in a subset of patients with heparin-induced thrombocytopenia (HITT). The pathogenic mechanisms underlying the variable occurrence of thrombosis in HITT is poorly understood. It was hypothesized that monocyte activation leading to tissue factor expression may play a role in promoting a thrombogenic state in HITT. This study demonstrates that a <prot>human platelet factor 4</prot> (<prot>PF4</prot>)/<prot>heparin-specific murine monoclonal antibody</prot> (<prot>KKO</prot>) binds to peripheral blood-derived human monocytes in a PF4-dependent manner. <prot>KKO</prot> and antibodies from patients with HITT induce monocytes to synthesize and secrete <prot>interleukin-8</prot> and induce cell-surface procoagulant activity, which is abrogated following treatment with antihuman tissue factor antibody. The findings suggest a novel mechanism by which <prot>PF4</prot>/heparin antibodies may promote a hypercoagulable state in patients with HITT. (Blood. 2001;98:1252-1254)</AbstractText>
