PLATELETS IN INFLAMMATORY DISEASES: MEDIATORS OF CLOTTING AND IMMUNE RESPONSES

Excessive and uncontrolled inflammation, coupled with thrombosis, are defining features of immune-mediated inflammatory disorders (IMIDs), contributing to organ damage, increased morbidity, and mortality. While platelets are primarily known for their role in clot formation, emerging research highlights their significant influence on inflammation and immune responses. Platelets engage with white blood cells and accumulate at injury sites, releasing cytokines and chemokines that attract neutrophils and monocytes, thereby amplifying the inflammatory response. In IMID patients, platelets are often activated by disease-specific triggers, with their activation levels correlating closely with disease activity. Beyond clotting, platelets exhibit immune cell-like behavior by engulfing pathogens, contributing to innate immunity. They also play a pivotal role in abnormal tissue healing and injury. Additionally, platelet-derived extracellular vesicles, laden with bioactive molecules, exacerbate inflammation, modulate immune responses, and promote thrombosis, thereby influencing disease progression. In autoimmune diseases, platelets not only support clotting and inflammation but also intensify autoimmunity by activating immune cells and perpetuating inflammatory feedback loops. Research into therapies targeting platelet activation and platelet-immune cell interactions presents promising strategies for managing IMIDs and reducing associated organ damage.