IFNβ has been shown to be required for maximal costimulatory molecule expression on peritoneal macrophages in response to LPS stimulation [16], whereas splenic cDCs which are deficient in the IFNαβ receptor (IFNαβR) and thus cannot respond to either type I IFN, show greatly enhanced expression of CD80 and CD86 in response to infection with Listeria monocytogenes in vivo[42]. The gene discussed is IFNAR2; the disease is infection.