Selective deletion of STAT1 in donor APCs does not prevent GVHD lethality, but global STAT1 deficiency expands pDCs. Lethally irradiated recipients received TCD MHC-mismatched BM from (A) CD11c Cre⁺ or Cre⁻ littermates followed by 1 × 10⁶ DLI from Cre⁻ donors on day +21 (B6 → C3H.HeNCr), (B) Lys Cre⁺ or Cre⁻ littermates followed by 1 × 10⁶ DLI from Cre⁻ donors on day +14 (B6.129 → C3H.HeNCr) or (C) CD19 Cre⁺ or Cre⁻ littermates followed by 1 × 10⁶ DLI from Cre⁻ donors on day +14 (B6.129 → C3H.HeNCr). All groups were followed for survival. (D) Lethally irradiated recipients received TCD miHA-mismatched BM from STAT1^+/+ or STAT1^−/− donors (129 → C3H.SW), and on day +14 immune reconstitution of CD11b⁻CD11c^intB220⁺ pDCs were enumerated by flow cytometry. (E) Comparison of the absolute numbers of pDCs from the BM and spleen of alloHSCT recipients by flow cytometry were calculated from total cell counts of each organ. (F) Lethally irradiated recipients received TCD miHA-mismatched BM from STAT1^+/+ or STAT1^−/− donors (CD45.2⁺ 129 → CD45.1⁺ B6), and on day +14 donor chimerism of pDCs were enumerated by flow cytometry. (G) pDCs were isolated from CD19 Cre^+/− × STAT1^flox/flox, Lys Cre^+/− × STAT1^flox/flox, CD11c Cre^+/− × STAT1^flox/flox, and a Cre^−/− × STAT1^flox/flox control to assess for expression of STAT1 RNA (100 bp) by RT-PCR. N = 5 to 7 mice/group, data are representative from 1 of 2 similar experiments. *P < .05, **P < .01.