scid HSCs are defective in self-renewal and niche occupancy. (A-C) Competitive repopulation assay of scid and Rag1^−/− HSCs. A total of 2 × 10⁶ BM from 8-week-old healthy WT, scid, or Rag1^−/− mice (CD45.2) were mixed with age-matched WT competitors (CD45.1) at 1:1 ratio, and transplanted into lethally irradiated WT recipients (CD45.1). Sixteen weeks after transplantation, donor chimerisms of myeloid cells (Mac1⁺) in the peripheral blood and HSCs (LSK) in the BM were analyzed and quantitated in panels B and C. Donor chimerisms of Mac1⁺ cells in the peripheral blood are calculated as the CD45.2⁺Mac1⁺ portion of the total Mac1⁺ cells. Donor chimerisms of LSK in the BM are calculated as the CD45.2⁺LSK portion of the total LSK. Error bars indicate SD; significance was determined by a Student 2-tailed t test. *P < .005. (D-F) Engraftment of WT HSC into unconditioned scid and Rag1^−/− mice. WT BM cells (5 × 10⁶; CD45.1) were transplanted into unconditioned WT, scid, and Rag1^−/− mice (CD45.2). Sixteen weeks after transplantation, donor chimerisms of multilineages in peripheral blood of recipients were analyzed by FACS, and representative results are shown in panel D. Myeloid chimerisms in the peripheral blood were quantitated in panel E, donor chimerism of myeloid cells is the CD45.1⁺Mac1⁺ portion of the total Mac1⁺ cells. Engraftment of transplanted WT BM HSCs (LSK) in the recipients were analyzed in panel F, donor chimerism of HSC is the CD45.1⁺LSK portion of the total LSK cells. Error bars indicate SD; the engraftment of WT BM into scid and Rag1^−/− mice was compared; significance was determined by a Student 2-tailed t test. *P < .01.