Fig 6.

IFN-λ signaling limits neutrophil abundance and severe skin pathology following HSV-1 infection. Eight- to twelve-week-old male and female WT and Ifnlr1^−/− mice were infected with 10⁶ FFU of HSV-1. (A and B) Dermatome lesions and adjacent healthy skin were collected at 4–8 dpi and analyzed by flow cytometry (three independent experiments per time point). (A) Representative histogram of WT and Ifnlr1^−/− lesions showing Ly6G^hi neutrophil gating strategy (CD45+, CD11b+, and Ly6G^hi) at 6 dpi. (B) Frequency of neutrophils (Ly6G^hi out of CD45+ CD11b+ live cells) for WT and Ifnlr1^−/− dermatome lesions and adjacent healthy skin. Significant differences in neutrophil frequency were determined using an unpaired t test. P values are reported with P < 0.05 considered to be statistically significant. (C and D) Inoculated flank skin was collected at 6 dpi and serial sections of the same skin lesion were processed for histology (six mice per genotype, two independent experiments). (C) H&E staining; the black arrow denotes a neutrophilic pustule, and the red arrow denotes diffuse neutrophilic infiltrate. (D) Anti-HSV-1 immunohistochemistry; viral antigen staining is denoted by black arrows. Scale bars are 100 µm.