CCR2-dependent recruitment of Ly6C⁺ cells, but not recruitment of Ly6G⁺ cells, is essential for <i>T. gondii</i> profilin-induced protection against <i>L. monocytogenes</i>.

<p>(A) CCR2 deficient (CCR2^−/−) mice (n = 4–5/group) were stimulated i.v. with 100 ng rPRF (grey) or PBS (black) 4 hours prior infection with ∼8×10³ CFU of <i>L. monocytogenes.</i> At 72 hours post <i>L. monocytogenes</i> infection, bacterial burdens of the spleen and liver, and percent weight change as compared to immediately prior to infection were quantified. Data shown are the mean ± SD from one of six independent experiments. (B) Mice depleted with anti-Gr-1 (Ly6c/Ly6G) MAb RB6-8C5 (n = 4/group) were stimulated i.v. with 100 ng rPRF (grey) or PBS (black) 4 hours prior infection with ∼200 CFU of <i>L. monocytogenes.</i> At 72 hours post <i>L. monocytogenes</i> infection, bacterial burdens of the spleen and liver, and percent weight change as compared to immediately prior to infection were quantified. Data shown are the mean ± SD from one of three independent experiments. (C) Mice depleted with anti-Ly6G MAb 1A8 (n = 4/group) were stimulated i.v. with 100 ng rPRF (grey) or PBS (black) 4 hours prior infection with ∼8×10³ CFU of <i>L. monocytogenes</i>. At 72 hours post <i>L. monocytogenes</i> infection, bacterial burdens of the spleen and liver, and percent weight change as compared to immediately prior to infection were quantified. Data shown are the mean ± SD from one of three independent experiments. (A–C) * indicates p<0.05, ** indicates p<0.01, *** indicates p<0.001, and **** indicates p<0.0001.