The detrimental effects of IFNγ are mediated through the donor T cell. TCD splenocytes from G-CSF–mobilized wt or IFNγR^−/− donors were added to purified wt or IFNγR^−/− T cells (n = 10 per group) and transplanted into irradiated (1100 rad) B6D2F1 recipients. TCD splenocytes from wt donors were transplanted into B6D2F1 recipients (n = 3) as non-GVHD controls. (A) Survival determined by Kaplan-Meier analysis. *P < .05 recipients of wt TCD splenocytes plus wt T cells and IFNγR^−/− TCD splenocytes plus wt T-cell grafts versus wt TCD splenocytes plus IFNγR^−/− T cells and IFNγR^−/− TCD splenocytes plus IFNγR^−/− T cells. (B) GVHD clinical scores were determined as a measure of GVHD severity in surviving animals **P < .01 recipients of wt TCD splenocytes plus wt T cells and IFNγR^−/− TCD splenocytes plus wt T-cell grafts versus wt TCD splenocytes plus IFNγR^−/− T cells and IFNγR^−/− TCD splenocytes plus IFNγR^−/− T cells. (C) Donor CD4⁺ and CD8⁺ T cells were quantified 12 days after SCT in B6D2F1 recipients of either wt TCD plus wt T cells (□; n = 6) or wt TCD plus IFNγR^−/− T cells (■; n = 6). *P < .05. (D) Levels of TNFα, IFNγ, and IL-5 were determined by cytokine bead array from sera 7 days after transplant. Data expressed as means plus or minus SE of individual animals (n = 9-10 in allogeneic groups, n = 3 in TCD). *P < .05, #P < .001 versus relevant control group.