Platelets in systemic lupus erythematosus: from hemostatic allies to pathogenic drivers.

Systemic lupus erythematosus (SLE) is a multisystem autoimmune disease; hematologic involvement is common and strongly associated with prognosis. Platelets-the second most abundant cellular component of peripheral blood-are anucleate cytoplasmic fragments. Their canonical roles include hemostasis, thrombosis, and vascular repair. More recently, platelets have emerged as regulators of innate and adaptive immunity that amplify inflammatory signaling and may facilitate tumor dissemination, suggesting underappreciated pathogenic roles in the initiation and progression of SLE. This review synthesizes platelet pathobiology in SLE and structures it into four modules: (i) pro-inflammatory actions of activated platelets; (ii) pathogenic effects of platelet-derived microparticles (PMPs); (iii) mechanisms by which platelets exacerbate lupus nephritis; and (iv) pathways linking platelets to SLE-associated cardiovascular disease. We also evaluate platelet-targeted therapeutic strategies and their translational prospects. Our aim is to provide a coherent framework for the platelet-SLE interface that informs mechanistic studies, guides biomarker development, and supports the design of more precise diagnostics and therapies.