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. 2015 Mar 9;125(4):1713–1725. doi: 10.1172/JCI78578

Figure 7. CXCR3 deprivation protects against prenatal L. monocytogenes infection–induced fetal wastage.

Figure 7

(A) Percentage of resorbed fetuses among C57BL/6 mice compared with isogenic CXCR3-deficient female mice 5 days after L. monocytogenes ΔactA (107 CFU) infection initiated midgestation (E11.5) during allogeneic pregnancies after mating with BALB/c males and controls without infection. (B) Percentage of resorbed fetuses among C57BL/6 female mice 5 days after L. monocytogenes ΔactA (107 CFU) infection initiated midgestation (E11.5) among C57BL/6 female mice during allogeneic pregnancies after mating with BALB/c males that were administered anti-CXCR3 compared with isotype control antibody (500 μg per mouse) 1 day prior to infection and controls without infection. (C) Representative FACS plots and composite data showing the percentage of fetal-OVA257–264-specific cells (CD90.1+) among CD8+ T cells recovered from the decidua or paraaortic lymph node 3 days after L. monocytogenes ΔactA (107 CFU) infection initiated midgestation (E11.5) for C57BL/6 female mice during allogeneic pregnancies after mating with by BALB/c-OVA males. Each symbol indicates the data from a single mouse, and these results, containing 4–8 mice per group, are representative of 3 independent experiments, each with similar results. Error bars represent mean ± 1 SEM.