Fig. 2: GPR37 confers protection against malaria infection.

a Experimental design for the mouse model of malaria infection. WT and Gpr37^−/− mice were treated with Plasmodium berghei (P.b.) sporozoites (10⁴, I.V.) and survival, rectal temperature, and serum IL-6 were measured as outcomes of infection. b Survival curves of WT and Gpr37^−/− mice. Sample sizes are indicated in brackets. c Time course of rectal temperature in WT and Gpr37^−/− mice. d Serum IL-6 levels in WT and Gpr37^−/− mice (n = 5/group). e Flow cytometry analysis of peripheral blood samples collected from WT and Gpr37^−/− mice 10 d after P.b. infection. Infected RBCs (iRBCs) were incubated with Hoechst dye (1 μg/ml) and CD45-FITC. Left upper panel: gating strategy to remove debris, aggregated cells, CD45⁺ WBCs, and small particles (<3 μm). Left down panel: representative images of RBCs sorted from WT or Gpr37^−/− mice 10 d after P.b. inoculation. Right panel: quantification of flow cytometry analysis at the indicated timepoints showing the proportion of iRBCs (Hoechst⁺ RBCs/total RBCs; 1 × 10⁶ RBC analyzed per sample, n = 5). f Giemsa staining was performed to detected iRBCs in WT and Gpr37^−/− mice 10 d after P.b infection. Left panel shows representative images. Right panel shows quantification of Giemsa-stained iRBCs (n = 13/group). Scale bar, 20 μm. Data are expressed as mean ± s.e.m. and statistically analyzed by Mantel–Cox test (b), 2-way ANOVA followed by Bonferroni’s post hoc test (c–e), and unpaired two-tailed t-test (f).