{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,23]],"date-time":"2026-10-23T13:04:18Z","timestamp":1792760658486,"version":"4.5.0"},"reference-count":100,"publisher":"Ovid Technologies (Wolters Kluwer Health)","issue":"15","content-domain":{"domain":["www.ahajournals.org"],"crossmark-restriction":true},"short-container-title":["JAHA"],"published-print":{"date-parts":[[2026,8,4]]},"abstract":"<jats:p xml:lang=\"en\">\n                    Platelets, classically defined by their hemostatic function, are increasingly recognized as immune effectors that shape chronic inflammation and vascular pathology in immune\u2010mediated inflammatory diseases. In conditions such as systemic lupus erythematosus, rheumatoid arthritis, and psoriasis, immune activation skews platelet adhesion, secretion, and procoagulant activity, while persistent interferon signaling and immune complex engagement (via receptors such as Fc\u03b3RIIA) amplify thromboinflammation. Platelets orchestrate leukocyte recruitment and endothelial activation through P\u2010selectin\/PSGL\u20101 (P\u2010selectin glycoprotein ligand\u20101) interactions, CD40 ligand, interleukin\u20101\u03b2, and the release of extracellular vesicles carrying cytokines and RNAs. Platelet involvement manifests differently across immune\u2010mediated inflammatory diseases. In systemic lupus erythematosus, they promote type I interferon priming, neutrophil extracellular trap formation, and endothelial dysfunction. In rheumatoid arthritis, they generate abundant synovial microparticles and systemic vascular changes. In psoriasis, they accumulate within skin lesions, enhance platelet\u2013leukocyte aggregation and activate proatherogenic endothelial responses. These pathways promote, independent of traditional cardiovascular risk factors, atherothrombosis including myocardial infarction, stroke, and venous thromboembolism. Limited translational data suggest that hydroxychloroquine may attenuate platelet activation and improve endothelial function. P2Y\n                    <jats:sub>12<\/jats:sub>\n                    inhibition may blunt interferon\u2010linked platelet RNA signatures and leukocyte\u2013platelet interactions. However, some therapies targeting inflammation, such as Janus kinase inhibitors, may promote thrombosis, the mechanisms of which are not fully known. Advances in multiomics, single\u2010cell and spatial profiling, and in\u00a0vivo models are delineating targets for intervention and enabling biomarker\u2010driven risk stratification. Collectively, platelets function as central translators between autoimmunity and atherothrombosis. Defining and modulating platelet\u2013immune crosstalk holds the potential to reduce cardiovascular risk in rheumatologic populations.\n                  <\/jats:p>","DOI":"10.1161\/jaha.125.047468","type":"journal-article","created":{"date-parts":[[2026,7,28]],"date-time":"2026-07-28T12:41:21Z","timestamp":1785242481000},"update-policy":"https:\/\/doi.org\/10.1161\/crossmarkpolicy","source":"Crossref","is-referenced-by-count":3,"title":["Platelet Activation and Autoimmunity: Mechanisms Linking Hemostasis and Cardiovascular Risk in Rheumatologic Disease"],"prefix":"10.1161","volume":"15","author":[{"ORCID":"https:\/\/orcid.org\/0009-0007-7259-3481","authenticated-orcid":false,"given":"Richard","family":"Ni","sequence":"first","affiliation":[{"name":"Leon H. 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