IFNG and Sepsis: At this point, it was evident that recruitment of effector cells to the skin of septic hosts was greatly reduced—an observation that could not be exclusively attributed to impairments in skin TRM Ag-dependent function to produce IFN-γ, the numerical loss of circulating cells that could be recruited to the inflamed peripheral site, or T cell intrinsic factor(s) that might prevent T cells exposed to sepsis or post-septic environment to follow inflammatory cues.