Anti-β2 glycoprotein I antibodies cause inflammation and recruit dendritic cells in platelet clearance

Scavenger phagocytes are mostly responsible for the in vivo clearance of activated or senescent platelets, In contrast to other particulate substrates, the phagocytosis of platelets does not incite proinflammatory responses in vivo. This study assessed the contribution of macrophages and dendritic cells (DCs) to the clearance of activated platelets, Furthermore, we verified whether antibodies against the beta2 Glycoprotein I (beta 2GPI), which bind to activated platelets, influence the phenomenon. DCs did not per se internalise activated platelets. In contrast, macrophages efficiently phagocytosed platelets, In agreement with the uneventful nature of the clearance of platelets in vivo. phagocytosing macrophages did not release IL-1 beta, TNF-alpha or IL-10. beta 2GPI bound to activated platelets and was required for their recognition by anti-beta 2GPI antibodies. DCs internalised platelets opsonised by anti-beta 2GPI antibodies. The phagocytosis of opsonised platelets determined the release of TNF-alpha and IL-1 beta by DCs and macrophages. Phagocytosing macrophages, but not DCs, secreted the antiinflammatory cytokine IL-10. We conclude that anti-beta 2GPI antibodies cause inflammation during platelet clearance and shuttle platelet antigens to antigen presenting DCs.