Dysregulation of platelets can contribute to inflammation and the formation of life-threatening blood clots. Researchers at the DZHK partner site in Munich have discovered a previously unknown protective mechanism in the spleen: it functions rather like a quality-control checkpoint, allowing resting platelets to pass on into the circulation while retaining and removing highly activated platelets. At the molecular level, this process involves a balance between activating signals from splenic tissue and inhibitory signals transmitted by the platelet receptor G6b. In highly activated platelets, the inhibitory signals are no longer sufficient to offset the activation: the platelets remain activated, adhere within the spleen, where they are removed by phagocytic cells. In animal models lacking this filtering mechanism, thrombosis, lung injury and pulmonary embolism were all more pronounced. Tissue analyses suggest that the spleen performs a similar filtering function in humans.
Link to publication:
Laun L, Leunig A, Zhang F, et al. Splenic regulation of systemic platelet activation state. Science. 2026;393(6817):eaec7230. doi:10.1126/science.aec7230
Link to press release:
Wie die Milz den Anteil aktivierter Blutplättchen im Blut reguliert
