Fig 7.

IFN-λ signaling suppresses neutrophil-mediated pathology to limit HSV-1 skin disease. (A) Experimental design for neutrophil depletions. (B–D) WT and Ifnlr1^−/− mice were infected with 10⁶ FFU of HSV-1. At 0, 2, and 4 dpi, mice were injected intraperitoneally with PBS, 250 µg of isotype control (IgG2a), or 250 µg of αLy6G (Clone 1A8). (B) Spleens were harvested at 6 dpi and analyzed by flow cytometry to confirm neutrophil depletion. (C) Skin lesions were photographed at 6 dpi, and lesion areas were measured using ImageJ. (D) Skin lesion severity was categorized based on the 6 dpi lesion area. (E–G) WT and Ifnlr1^−/− mice were infected with 10⁶ FFU of HSV-1, and at 6 dpi, skin lesions were photographed and analyzed by flow cytometry. (E) Representative plots and gating strategy for neutrophil phenotyping markers LFA-1 and CD63 (percentage of CD45+ CD11b+ Ly6G+). (F) Frequency of CD63+ neutrophils. (G) Frequency of LFA-1+ CD63− neutrophils. Differences in lesion area and viral load were compared by the Mann-Whitney U test, and differences in categorical skin disease were compared by the Cochran-Armitage test. Neutrophil frequencies were compared by unpaired t test. P values are reported with P < 0.05 considered to be statistically significant. Data are combined from two to three independent experiments.