The activation of the transcription factor NFAT in platelets regulates neutrophil extracellular traps during colitis 2644

Abstract Description Non-immune cells contribute to induce an effective immune response and recent studies showed that platelets are major players in the modulation of the inflammation. Although platelets are anucleated cells, we recently found that the transcription factor NFAT modulates the activation of platelets and controls their hemostatic and inflammatory activity (Immunity, 2022). In particular, we showed that inhibition of NFAT activation in platelets boosts the anti-microbial functions of neutrophils and their capacity to release neutrophils extracellular traps in the context of sepsis. Mechanistically, we showed NFAT activation determine secondary granule release by platelets, the extent of their aggregation and activation, and a feed-forward loop with NET induction. Whether NFAT activation in platelets can regulate NETosis in the context of chronic inflammatory diseases remains a mystery. Here we focused on inflammatory bowel diseases (IBD), a group of diseases whose etiology is still a matter of debate. In the context of a mouse model of colitis, we investigated whether NFAT activation in platelets regulates NET induction during intestinal inflammation and its impact on disease progression. Funding Sources Crohn’s and colitis foundation research fellowship award Topic Categories Innate Immune Responses and Host Defense: Cellular Mechanisms (INC)