Fig 2: Enhanced allergic asthma in Cc10−/− mice post HDM exposure. A Western blot showing absence of CC10 in Cc10−/− lung tissue. B HDM sensitization/challenge protocol for wild type and Cc10−/− mice, with PBS controls. Analysis occurred 2 days post-final challenge. C Airway resistance to MCh increments; normalized to baseline (n = 6/group). D, E BALF cell counts (n = 6/group). F ELISA quantification of HDM-specific IgE (n = 6/group). G Lung histology stained with H&E or PAS; scale bar = 200 μm. H Quantitative assessment of inflammatory infiltration and goblet cell hyperplasia (n = 6/group). I Quantification analysis for Muc5ac mRNA expression in mice lung tissues (n = 4/group). J ELISA determination of IL-4, IL-5, and IL-13 in BALF (n = 6/group). Data are mean ± SEM. P values: one-way ANOVA with Games-Howell test (D–I), two-way ANOVA (C). *P < 0.05, **P < 0.01, ns not significant

Fig 3: Eosinophil deficiency prevents chronic skin inflammation.(A) Representative clinical course in 4get (WT) and dblGATA-1 4get (KO) mice infected with L. mexicana (WT n = 12; KO n = 14, 1 of 4 independent experiments). (B) Parasite load determined by limiting dilution analysis of the respective organs from WT and KO mice (day 49: n = 4 mice per group for foot skin, dLN, and spleen; day 95–125: foot skin WT n = 10, KO n = 8; dLN WT n = 9, KO n = 11; spleen WT n = 7, KO n = 12, 1–3 independent experiments). (C) Representative clinical course of L. mexicana-infected C57BL/6 mice treated with 500 µg of either isotype control or anti-IL-5 antibody on days 5 and 12 p.i. (n = 12 mice per group, 1 of 2 independent experiments). (D) Parasite load determined by limiting dilution analysis of the respective organs, comparing isotype control and anti-IL-5 treatment (day 81–85: foot skin isotype n = 8, anti-IL-5 n = 6; dLN isotype n = 8, anti-IL-5 n = 7; spleen isotype n = 7, anti-IL-5 n = 8; day 145: foot skin, dLN, and spleen isotype n = 3, anti-L-5 n = 4, 3 independent experiments). (E) Quantification of Ifng, Il4, Il10 and Il13 mRNA expression by qRT-PCR analysis of L. mexicana-induced skin lesions from WT and KO mice (exact n values vary by gene and time point and are provided in Appendix Table S2, 1–2 independent experiments). Data are mean ± SEM (A, C) or mean ± s.d. (B). ND: not detectable. Information regarding the exact p values and the statistical tests performed is provided in the Appendix Table S1. Source data are available online for this figure.

Fig 4: ILC2s orchestrate eosinophil responses during chronic skin inflammation.(A) Serum IL-5 levels measured by ELISA in Rorαflox/flox (WT) and RorαΔTek (KO) mice infected with L. mexicana (day 0: n = 4; day 6: WT n = 5, KO n = 7; day 14: WT n = 8, KO n = 7, 2 independent experiments). (B) Left, representative flow cytometric analysis of isolated skin cells from WT and KO mice infected with L. mexicana. Right, quantification of the respective population (day 0: n = 3; day 6: WT n = 2, KO n = 2; day 14: WT n = 2, KO n = 2, one experiment; skin data points were derived from samples pooled from two mice). (C) Right, representative flow cytometric analysis of cells isolated from bone marrow and blood of WT and KO mice infected with L. mexicana. Left, quantification of the respective population and organ (exact n values vary by organ and time point and are provided in Appendix Table S2, 2 independent experiments). Data are mean ± s.d. Information regarding the exact p values and the statistical tests performed is provided in the Appendix Table S1. Source data are available online for this figure.