STAT1^−/− mice have BM-derived pDCs that produce low levels of IFNα and nitrogen free radicals, which decrease activation of antigen-specific T cells after alloHSCT. (A) pDCs were isolated from the BM of nontransplanted (naïve) STAT1^+/+ and STAT1^−/− mice, stimulated with control ODN vs CpG ODN and analyzed for IFNα production by ELISA. (B) Splenic pDCs were isolated from irradiated recipients of WT, IRF9^−/−, IFNγR1^−/−, or STAT1^−/− BM on day +14, and then were analyzed for 3-nitrotyrosine production in culture ex vivo. (C) Lethally irradiated recipients received TCD miHA-mismatched BM from STAT1^+/+ or STAT1^−/− donors (129 → C3H.SW), and on day +14 pDCs were isolated from BM, and were pulsed with WT-1 peptide, and then were activated by CpG. T cells from WT-1 TCR transgenic mice were cocultured with the activated, WT-1 expressing pDCs and intracellular IFNγ expression was enumerated by flow cytometry. N = 5 mice/group, data are representative from 1 of 2 similar experiments. *P < .05, ***P < .001.