ILC1-derived IFN-γ mediates cDC1-dependent host resistance against Toxoplasma gondii

Host resistance against intracellular pathogens requires a rapid IFN-γ mediated immune response. We reveal that T-bet-dependent production of IFN-γ is essential for the maintenance of inflammatory DCs at the site of infection with a common protozoan parasite, . A detailed analysis of the cellular sources for T-bet-dependent IFN-γ identified that ILC1s, but not NK or T1 cells, were involved in the regulation of inflammatory DCs via IFN-γ. Mechanistically, we established that T-bet dependent ILC1-derived IFN-γ is critical for the induction of IRF8, an essential transcription factor for cDC1s. Failure to upregulate IRF8 in DCs resulted in acute susceptibility to infection. Our data identifies that ILC1-derived IFN-γ is indispensable for host resistance against intracellular infection via maintaining IRF8+ inflammatory DCs at the site of infection.