Third, we observed that IFN-γ deficiency in donor T cells as well as reduction of IFN-γ+ Th/Tc1 cells by steroid treatment led to depletion of CX3CR1hi MNP in the gut tissue of GVHD recipients; in addition, lack of donor T-derived IFN-γ led to CX3CR1hi MNP upregulating expression of PD-1 and becoming more sensitive to tissue PD-L1-induced apoptosis. This evidence concerns the gene IFNG and graft versus host disease.