Secretion of type I IFN increases susceptibility to Listeria by inducing apoptosis of T cells and macrophages [16] [17] [18] . In accordance, mice deficient of IFNAR are more resistant to Listeria and show decreased T cell apoptosis in the spleen during infection [17, 19, 20] . Moreover, type I IFN are able to down regulate IFN-c receptor thereby suppressing macrophage activation and increasing host susceptibility to Listeria infection [21, 22] .