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. Author manuscript; available in PMC: 2024 Apr 22.
Published in final edited form as: Mucosal Immunol. 2024 Jan 20;17(2):182–200. doi: 10.1016/j.mucimm.2024.01.003

Fig. 4.

Fig. 4

Blockade of PSGL-1 signaling results in decreased neutrophil response during oropharyngeal candidiasis. (A) Representative flow cytometry plots of neutrophil populations (GR-1+) in tongue tissue on Day 1 of OPC between WT Sham, WT OPC, Isotype control OPC, and α-PSGL-1 OPC mice. (B) Quantification of neutrophil flow cytometry data from (A). N = minimum three mice per cohort, analyzed by one-way ANOVA. Mean ± SEM. (C) Representative flow cytometry plots of neutrophil populations (GR-1+) in tongue tissue on Day 1 of OPC between WT OPC, PF4-iDTR OPC, and platelet-transfused PF4-iDTR mice. (D) Quantification of neutrophil flow cytometry data from (C). N = minimum four mice per cohort, analyzed by one-way ANOVA. Mean ± SEM. (E) Fungal burden (CFU/g) of platelet-transfused PF4-iDTR murine tongue tissue on Day 1 of OPC. Results representative of two independent experiments. **p > 0.01, ***p > 0.001, ****p < 0.0001, n.s. is not significant. ANOVA = analysis of variance; CD = cluster of differentiation; OPC = oropharyngeal candidiasis; PSGL-1 = P-selectin glycoprotein ligand-1; SEM = standard error of the mean; WT = wild-type.