Figure 4
Figure 4. The developmental defect of NK cells in CXCR4 conditionally deficient mice is cell-intrinsic. Ly5.2+/Ly5.1− bone marrow cells from MxCre/CXCR4f/wt or MxCre/CXCR4f/null mice were mixed with Ly5.2−/Ly5.1+ wild-type bone marrow cells and transplanted into lethally irradiated normal Ly5.2−/Ly5.1+ wild-type recipients. At 12 weeks after transplantation, mice were treated with pIpC. At 15 week after final pIpC treatment, recipient mice were analyzed by flow cytometry. (A) The numbers of donor-derived Ly5.2+CD3−NK1.1+DX5− iNKs and Ly5.2+CD3−NK1.1+DX5+ mNKs; n = 4. *P < .05. **P < .01. (B) Quantitative RT-PCR analysis of mRNA expression of CXCR4 in NKPs, CD3−NK1.1+DX5− iNKs, and CD3−NK1.1+DX5+ mNKs in the bone marrow from wild-type mice. Data are normalized to GAPDH levels; n = 3.

The developmental defect of NK cells in CXCR4 conditionally deficient mice is cell-intrinsic. Ly5.2+/Ly5.1 bone marrow cells from MxCre/CXCR4f/wt or MxCre/CXCR4f/null mice were mixed with Ly5.2/Ly5.1+ wild-type bone marrow cells and transplanted into lethally irradiated normal Ly5.2/Ly5.1+ wild-type recipients. At 12 weeks after transplantation, mice were treated with pIpC. At 15 week after final pIpC treatment, recipient mice were analyzed by flow cytometry. (A) The numbers of donor-derived Ly5.2+CD3NK1.1+DX5 iNKs and Ly5.2+CD3NK1.1+DX5+ mNKs; n = 4. *P < .05. **P < .01. (B) Quantitative RT-PCR analysis of mRNA expression of CXCR4 in NKPs, CD3NK1.1+DX5 iNKs, and CD3NK1.1+DX5+ mNKs in the bone marrow from wild-type mice. Data are normalized to GAPDH levels; n = 3.

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