Platelets form special structures called PITT (Platelet-derived Integrin- and Tetraspanin-enriched Tethers), which are enriched with integrin αIIbβ3 and tetraspanin CD9[2][3][6]. These PITTs arise from disintegration complexes (DISCs), into which integrins, tetraspanins and signaling molecules including ribosomes and RNA are organized[1][2][3]. PITTs detach from platelets and deposit on immune cells and vessel walls, increasing inflammation and tissue damage[6][7]. The discovery was confirmed in blood samples from patients with severe sepsis, bacterial infections and COVID-19, where platelets lost surface αIIbβ3 and formed fibrous tethers[2][6]. In murine models, PITTs reduce lung neutrophil recruitment, inflammation and tissue damage in the absence of vWF[2]. PITTs are formed under the influence of mechanical stress and antibodies against αIIbβ3, which leads to their deposition on blood vessels[2][6]. The study shows that PITTs switch platelets from hemostatic to thrombo-inflammatory function[1][3]. Published in Science (2026, Volume 391).[4][6]