Figure 5
Figure 5. T-bet deficiency in innate cells and nonresponding lymphocytes does not prevent CXCR3 induction in T-bet–sufficient B cells. Chimeras were constructed by transfer of CD45.1+ NP-specific B1.8hi B cells and OTII cells or both OTI + OTII cells either into CD45.2+ WT C57BL/6 or congenic T-bet−/− mice. The chimeras were immunized in both footpads with alumNP-OVA, and 7 days later popliteal LN cell suspensions were prepared as in Figure 1. The percentage of CXCR3+ B1.8hi AFCs (CD138+B220intCD45.1+ cells) and GC B cells (B220+GL7+Fas+ cells) in these suspensions was assessed by flow cytometry. The bar chart represents the mean ± SD (percentage) B1.8hi cells that were CXCR3+. Open bars represent data from WT recipients; and closed bars, data from T-bet−/− recipients. Data are derived from 2 independent experiments with a total of 6 mice in each group. The significance of differences are assessed by 2-tailed Mann-Whitney nonparametric statistics. NS indicates not significant.

T-bet deficiency in innate cells and nonresponding lymphocytes does not prevent CXCR3 induction in T-bet–sufficient B cells. Chimeras were constructed by transfer of CD45.1+ NP-specific B1.8hi B cells and OTII cells or both OTI + OTII cells either into CD45.2+ WT C57BL/6 or congenic T-bet−/− mice. The chimeras were immunized in both footpads with alumNP-OVA, and 7 days later popliteal LN cell suspensions were prepared as in Figure 1. The percentage of CXCR3+ B1.8hi AFCs (CD138+B220intCD45.1+ cells) and GC B cells (B220+GL7+Fas+ cells) in these suspensions was assessed by flow cytometry. The bar chart represents the mean ± SD (percentage) B1.8hi cells that were CXCR3+. Open bars represent data from WT recipients; and closed bars, data from T-bet−/− recipients. Data are derived from 2 independent experiments with a total of 6 mice in each group. The significance of differences are assessed by 2-tailed Mann-Whitney nonparametric statistics. NS indicates not significant.

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