Inhibiting NF-κB signaling in AA mice reduces CXCR4 expression in T cells and attenuates AA. F1 hybrid mice were irradiated only (γIR control) or AA was induced with 5 × 10⁷ WT C57BL/6 splenocytes. Mice were treated with DMSO (BMF + DMSO), DHMEQ (BMF + DHMEQ), or Bay11 (BMF + Bay11). In some mice, AA was induced with 5 × 10⁷ p50^−/− splenocytes (BMF p50^−/−). On day +17 postdisease induction, mice were harvested and (A) total BM cellularity was determined by trypan blue exclusion; n = 12 mice per group. (B) Representative hematoxylin and eosin staining of sternum from 1 representative animal each of irradiation control (γIR control), DMSO-treated AA mouse (BMF + DMSO), DHMEQ-treated AA mouse (BMF + DHMEQ), Bay11-treated AA mouse (BMF + Bay11), and 1 mouse that received p50^−/− splenocytes (BMF p50^−/−). Scale bar = 200 μM. (C) Percentages of BM-infiltrating CD4⁺ and CD8⁺ T cells in irradiation controls or AA mice that received DMSO, DHMEQ, Bay11, or p50^−/− splenocytes were determined by flow cytometry; n = 12 mice per group. (D) MFI of CXCR4 protein expression on BM-infiltrating CD4⁺ and CD8⁺ T cells of AA mice that received DMSO, DHMEQ, Bay11, or p50^−/− splenocytes was assessed by flow cytometry and compared with CXCR4 MFI on BM-infiltrating T cells of irradiation controls; n = 12. (E) Kaplan–Meier survival estimates of AA mice whose disease was induced with WT splenocytes and treated with DMSO (n = 8) or Bay11 (n = 7), beginning on day +7 postdisease induction and continuing until day +17 postdisease induction. Data are the mean ± SEM, and analyzed using one-way ANOVA plus Tukey post-test or log-rank test for survival estimates. *P < .05; **P < .01; ***P < .001.