The role of platelet in systemic lupus erythematosus

Systemic lupus erythematosus (SLE) is a systemic autoimmune disease with manifestations ranging from mild skin symptoms to severe organ and neurological involvement. Thrombosis is a major complication and leading cause of mortality, though its mechanisms remain unclear. Emerging evidence highlights platelets, beyond their hemostatic role, as central players in SLE pathogenesis. This narrative review summarizes platelet-driven pathways in SLE, emphasizing their roles in thrombosis and immune regulation. Platelets interact with immune complexes, complement, and infectious agents, triggering activation and the release of mediators and microparticles. These processes increase circulating autoantigens and promote both thrombosis and autoimmune responses. Understanding these non-hemostatic platelet functions offers new insight into SLE mechanisms and may guide future platelet-targeted therapies.