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We found that ligation of \u03b1IIb\u03b23 by von Willebrand factor or fibrin under flow triggered its accumulation in plasma membrane extensions or \u201cplatelet-derived integrin- and tetraspanin-enriched tethers\u201d (PITTs). PITTs remained anchored to leukocytes or endothelial cells, whereas the partially \u03b1IIb\u03b23-deficient platelet body detached. Although still responsive to stimuli, \u03b1IIb\u03b23-deficient platelets did not support thrombus formation. PITTs promoted leukocyte activation and vascular inflammation in mouse models of infection and endotoxemia, and \u03b1IIb\u03b23 blockade reduced immune-mediated tissue damage. In patients with sepsis, COVID-19, or severe infections, PITT formation and platelet \u03b1IIb\u03b23 loss correlated with disease severity and adverse outcomes. 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