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. 2022 Feb 23;13:821658. doi: 10.3389/fimmu.2022.821658

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Copyright © 2022 Krammer, Yang, Zimmermann, Xepapadaki, Geppert, Papadopoulos and Finotto

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Lung ILC2s in an ovalbumin (OVA)-induced asthma model with intranasal rIL-3 application. (A) Experimental design for the induction of allergic asthma in wild-type (WT) mice treated with rIL-3 for the analysis of lung ILC2s. (B) Cartoon on the differentiation of different ILC2 subpopulations. (C–F) Flow cytometry analysis of ILC2 after in vitro differentiation. Flow cytometry analysis of lung ILC2s (%) (C, D); flow cytometry analysis of GATA3+ ST2^int. ILC2 (E, F) in the lung of WT mice with asthma and with and without additional rIL-3 treatment during sensitization or challenge phase (n = 6/7/7). (G) Cartoon on the mechanism of IL-3 involvement in ST2 shedding from ILC2. Data are presented as means ± SEMs. One-way ANOVA or Kruskal–Wallis test was used to calculate statistical significance. *p ≤ 0.05; **p ≤ 0.01.