scRNAseq Dataset of lungs from WT and Clec1a KO mice following primary or secondary E. coli lung infection

Pneumonia is associated with significant morbidity and mortality and is the leading cause of hospitalization and death worldwide. Sepsis exhibits phases of enhanced inflammation, alternating with immune suppression. Sepsis-induced immunosuppression is characterized by a deep remodelling of the myeloid immune compartment, leaving patients vulnerable to more severe forms of secondary infections. Pattern Recognition Receptors (PRRs), such as the C Type Lectin Receptors (CLRs) family, are able to respond to a wide variety of endogenous and exogenous ligands, modulating a plethora of innate responses. We previously described the CLR CLEC-1, as a receptor of necrotic cells expressed by myeloid cells such as conventional Dendritic Cells type I (cDC1), and able to limit antigen presentation and downstream T cell response. Therefore, we evaluated the role of this novel immune checkpoint during the initial pro-inflammatory phase, and in the later inflammation resolution phase of sepsis. To do so, we performed E. coli lung primary and secondary infections in C57BL6 Clec1a deficient mice and analysed the immune response at day 1 and 3 following infections by scRNAseq.