Fig. 7: Defective Axl engagement upregulates macrophage-mediated immunity.

Male Axl^−/− (open triangle) and WT (closed triangle) mice were infected sc with T. cruzi parasites. Normal Axl^−/− and WT mice were used as controls. At 14 dpi, splenocytes and peritoneal exudate cells were analysed by flow cytometry. a, b Percentages and absolute numbers of F4/80⁺ macrophages and CD11b⁺Ly6C⁺ monocytes from the spleens are represented for each mouse. c Representative plots show the expression of extracellular CD301 and intracellular IL-12p35, iNOS, and Arg1 in F4/80⁺ splenocytes. The graphs depict the percentages of CD301⁺IL12p35⁺ cells and iNOS⁺ macrophages. d Percentages and absolute numbers of F4/80⁺ peritoneal macrophages. e NO production in infected WT and Axl^−/− mice, as evaluated in 5 mL-diluted peritoneal exudates. f Parasite load of in vitro-infected peritoneal macrophages. The means and SEM of n = 4 normal WT mice, n = 4 Axl^−/− normal mice, n = 7 infected WT mice, and n = 7 infected Axl^−/− are shown. Significant differences, as analysed (in a and b) by ANOVA followed by Bonferroni posttest (noninfected versus infected mice; Axl^−/− versus WT mice) or (in c, d, e, and f) by unpaired Student’s t-tests (infected Axl^−/− versus infected WT mice) are indicated as for ^*P < 0.05, ^**P < 0.01, ^***P < 0.001, and ^****P < 0.0001.