Fig 1: Platelets from patients with COVID-19 activate monocytes through surface interaction and TF-mediated signaling. (A) Monocytes from healthy volunteers were incubated with platelets from patients with severe COVID-19 for 18 hours in the presence of anti-P-selectin (anti-CD62P) neutralizing antibody, the anti-aIIb/ß3 antibody abciximab, anti-TF clone 10H10, anti-TF clone 5G9, or isotype matched IgG. The percent inhibition on platelet-monocyte aggregate formation (CD41+ monocytes), monocyte CD16 expression, and on cytokine release is shown for each condition. (B-C) Control monocytes were exposed to platelets from patients with severe COVID-19 in the presence of the antiplatelet drugs aspirin, clopidogrel, or DMSO (vehicle). The percent inhibition on platelet-monocyte aggregate formation, monocyte CD16 expression and on cytokine release (B) and the percentage of monocytes expressing CD16 (C) are shown for each condition. Bars represent mean ± standard error of the mean of monocytes exposed to platelets from 3 to 6 independent patients with COVID-19. *P < .05 compared with isotype-matched IgG (A) or vehicle (B-C).