Fig 1. Poly(I:C) activates innate immune responses in a dose-dependent manner and inhibits IL-33 induced eosinophilia and ILC2 proliferation.

A. Experimental setup of an acute lung inflammation model that illustrates the animal groups, the corresponding treatment regimen and timeline (upper panel) and weigh changes following treatment as indicated. Error bars represent SEMs. Statistics of the weight changes was determined using the Two-Way ANOVA. The dot lines (animal groups treated with either PBS or increased amount of Poly(I:C) without IL-33, ^### p < 0.001, ^#### p < 0.0001); the sold lines (animal groups treated with PBS or increased amount of Poly(I:C) with IL-33, ** p < 0.01, ****p < 0.0001). B. Transcriptional induction of gene expressions by Poly(I:C) in mouse lungs. C. Groups of mice as indicated were treated with PBS, IL-33 in presence of increased doses of Poly(I:C) as indicated. Bronchoalveolar lavage fluid (BALF) was collected and analyzed for differential immune cell types. The result is a pool of two independent experiments. (n = 3–5 per group as indicated with open circles). D. Administration of Poly(I:C) in a dose-dependent manner reduced the percentage and number of lung-eosinophils after exposure to IL-33. (n = 3–5 per group as indicated with open circles). E. Poly(I:C) treatment decreased the number of lung-ILC2 cells after exposure to IL-33 in a dose-dependent manner. (n = 3–5 per group as indicated with open circles). Unless otherwise indicated, P value was determined using Mann-Whitney test, P value ≥0.05 was not considered statistically significant [N.S.]). * p < 0.05, ** p < 0.01.