Using Xcr1Cre-Gfp Rosa26LSL-DTA Apoe–/– model and Xcl1–/– Apoe–/– mouse model reveal an essential non-redundant role for the XCL1-XCR1 axis in cDC1-mediated atherogenesis.
Inhibition of the UFD-1-NPL-4 complex activates immune responses in Caenorhabditis elegans that reduce gut pathogen load but simultaneously compromise host survival.