摘要：SummarySepsis is a leading cause of morbidity and mortality associated with significant impairment in memory T cells. These changes include the upregulation of co-inhibitory markers, a decrease in functionality, and an increase in apoptosis. Due to recent studies describing IL-27 regulation of TIGIT and PD-1, we assessed whether IL-27 impacts these co-inhibitory molecules in sepsis. Based on these data, we hypothesized that IL-27 was responsible for T cell dysfunction during sepsis. Using the cecal ligation and puncture (CLP) sepsis model, we found that IL-27Rα was associated with the upregulation of TIGIT on memory CD4+T cells following CLP. However, IL-27 was not associated with sepsis mortality.Graphical AbstractDisplay OmittedHighlights•Numbers of IL-27Rα+memory T cells are decreased following cecal ligation and puncture•TIGIT is expressed on more IL-27Rα+versus IL-27Rα−memory CD4+T cells during sepsis•Il27ra−/−and WT T cells exhibit similar effector function and apoptosis during sepsis•IL-27 signaling does not impact sepsis mortalityMolecular Biology; Immunology
