Absence of Clec1a in murine cDC1s decrease IFN responses to necrotic cells

Interferons (IFNs) are proteins that signal and play a critical role in health and disease. IFNs play a protective role gainst pathogens such as during viral, bacteria and fungal infections, but can also mediate many inflammatory and autoimmune diseases. IFNs are characterized by time-dependent activities that can drive opposing outcomes so IFN responses need to be carefully balanced to prevent deleterious effects and for the return to homeostasis. We previously characterized the C-type lectin receptor CLEC-1 as a receptor of necrotic cells particularly expressed by cDC1s. Here, we showed that the absence of Clec1a in cDC1s decreases the IFN responses to necrotic cells but not to pathogen such as E. Coli. These results suggest that CLEC-1 in cDC1s potentiates IFN signaling in response to necrotic cells to finely regulate downstream immunity.