CLEC-1 promotes early IFN response in cDC1s and favors immune dysregulation during sepsis in mice
Summary Sepsis is a life-threatening organ dysfunction caused by a dysregulated host immune response, characterized by both hyperinflammation and immunosuppression. Here, we show that the absence of the C-type lectin receptor CLEC-1—expressed particularly by lung cDC1s—improves mouse recovery following E. coli infectio...