Deletion of IFNAR attenuates the reconstitution defects of NFAT5-deficient hematopoietic progenitors in BMT. (A) Donor-derived (CD45.2⁺) reconstitution of lineage^neg bone marrow (upper panel), and percentage and number of LSK cells (middle and bottom panels) 13 weeks after primary BMT with the indicated genotypes. (B) Percentage and number of donor-derived hematopoietic progenitor populations in the bone marrow of mice reconstituted with bone marrow of the indicated genotypes. Results for HSC and MPP are from 2 independent transplants, each with 1 donor bone marrow of the respective genotype and 5 to 7 recipients. LT-HSC and ST-HSC distribution was analyzed in 1 experiment. (C) Percentage of donor-derived apoptotic cells (annexin V⁺ DAPI⁻) in hematopoietic progenitor subsets 13 weeks after BMT of the indicated genotypes. (D-E) Donor-derived reconstitution of bone marrow hematopoietic progenitor subsets (E) and blood platelets (D, plateletcrit [PCT], blood platelets per mL, and platelet distribution width [PDW]) after secondary transplant with bone marrow of the indicated genotypes. Secondary transplants used bone marrow from 1 of 2 experiments shown in panel B, using a pool of 6 donors of each genotype to reconstitute 6 to 7 secondary recipients. (F) Survival of mice in tertiary transplants with bone marrow cells derived from the indicated genotypes. Tertiary transplants used donor bone marrow pools of secondary transplanted mice from panel E to reconstitute 7 recipients. Results are shown as mean ± SEM. Statistical significance is shown for comparisons between the indicated genotypes, and was determined with an unpaired t test for panels A-E and a log-rank Mantel-Cox test for panel F. ∗P < .05, ∗∗P < .01, ∗∗∗P < .001. P values < .1 are also indicated. LT, long-term; ST, short-term.