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Войти в исследования Science (New York, N.Y.) · 2026
Platelet-derived integrin- and tetraspanin-enriched tethers exacerbate severe inflammation.
СтатьяНазвание и аннотация: Перевод в очереди
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Kusch Charly, Stegner David, Weiss Lukas J, Nurden Paquita, Burkard Philipp, Johnson Denise, Bergmeier Wolfgang, Onursal Ceylan, Navarro Stefano, Hackenbroch Christian, Pfeiffer Dennis, Bonfiglio Sabrina Ivana, Meub Mara, Gross Carina, Schenk Joachim, Fumagalli Valeria, Mott Kristina, Bender Markus, Iannacone Matteo, Andres Oliver, Kastenmüller Wolfgang, Heinze Katrin G, Sauer Markus, Schulze Harald, Ley Klaus, Nurden Alan T, Nieswandt Bernhard
Аннотация
Platelet integrin αIIbβ3 is essential for hemostasis, thrombosis, and inflammation. We found that ligation of αIIbβ3 by von Willebrand factor or fibrin under flow triggered its accumulation in plasma membrane extensions or "platelet-derived integrin- and tetraspanin-enriched tethers" (PITTs). PITTs remained anchored to leukocytes or endothelial cells, whereas the partially αIIbβ3-deficient platelet body detached. Although still responsive to stimuli, αIIbβ3-deficient platelets did not support thrombus formation. PITTs promoted leukocyte activation and vascular inflammation in mouse models of infection and endotoxemia, and αIIbβ3 blockade reduced immune-mediated tissue damage. In patients with sepsis, COVID-19, or severe infections, PITT formation and platelet αIIbβ3 loss correlated with disease severity and adverse outcomes. We propose that PITTs are proinflammatory structures that amplify immune responses while contributing to platelet dysfunction in thrombo-inflammatory disease.