Figure 3.

Migration of T bodies to the BM of preconditioned mice is mediated in part by CXCR4. SCID mice (n = 3 mice per group) were irradiated with 2 Gy TBI or were injected with 200 mg/kg cyclophosphamide, 24 hours before i.v. administration of erbB2-specific CR–bearing lymphocytes. T bodies were preincubated for 30 minutes on ice with mAb against CXCR4 (αCXCR4), irrelevant control mAb against human TfR (αTfR), or no antibody (none) and then were injected systemically into the mice. After 24 hours, BM was extracted and the number of human lymphocytes was measured by FACS analysis (detecting GFP-positive T bodies in the irradiation experiment and CFSE-labeled cells in the cyclophosphamide experiment). Treatment with anti-CXCR4 was significantly different from control treatment (anti-TfR) for both irradiated mice (*P = 0.003) and cyclophosphamide-treated mice (**P = 0.009) and was significantly different from no antibody treatment (P = 0.01 and P = 0.0002, respectively).