Inhibiting CXCR4 in AA mice reduces T-cell homing to the BM. (A) Representative histograms of CXCR4 expression on splenocytes from WT C57BL/6 mice, poly:IC-treated Mx1-cre^+/− mice (Mx1-cre^+/−; Mx1-cre only control), poly:IC-treated CXCR4^fl/flMx1-cre^−/− mice (CXCR4^fl/flMx1-cre^−/−; poly:IC control), or poly:IC-treated CXCR4^fl/flMx1-cre^+/− mice (CXCR4^fl/flMx1-cre^+/−; CXCR4^−/−). (B) Donor splenocytes from (A) were used to induce AA in F1 recipient mice (BMF). On day +17 postdisease induction, percentages of BM-infiltrating CD4⁺ and CD8⁺ T cells in AA mice were assessed by flow cytometry and compared with mice that were irradiated only (γIR control); n = 7 mice per group. (C) Mice were induced with AA (BMF), and from days +7 to +16 postdisease induction, were treated with PBS (BMF + PBS) or with the CXCR4 antagonist, AMD3100 (BMF + AMD3100). Percentages of BM-infiltrating CD4⁺ and CD8⁺ T cells in AA mice were determined as in (B); n = 11 mice per group. (D-E) F1 hybrid mice were irradiated only (γIR control) or AA was induced by transferrin 5 × 10⁷ WT C57BL/6 splenocytes (BMF). On day +17 postdisease induction, the MFI of CXCR4, CXCR7, CX3CR1, CCR5, and CXCR3 on (D) CD4⁺ and (E) CD8⁺ T cells from the spleens and BM of AA mice or irradiation controls was assessed by flow cytometry. Expression was relative to γIR control and was calculated by dividing the MFI of BMF samples by the mean MFI of γIR controls; n = 8 mice per group. Data are the mean ± SEM, and were analyzed by one-way ANOVA plus Tukey post-test. *P < .05; **P < .01; ***P < .001.