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. 2024 Jul 16;10:324. doi: 10.1038/s41420-024-02096-y

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© The Author(s) 2024

Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons licence, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons licence, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons licence and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this licence, visit http://creativecommons.org/licenses/by/4.0/.

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Fig. 4 — Development of ILC2s: CCR2⁺ ILC2 in the lung is initially derived from bone marrow ILC2 differentiated from ILCP; during development, lung ILC2 migrates to the intestine and the phenotype shifts from CCR2⁺ CCR4⁻ to CCR2 ⁺ CCR4⁺ and then to CCR2^-CCR4⁺. Tissue homeostasis: in a stable tissue microenvironment, lung-intrinsic ILC2 stably expresses CCR2 but not CCR4, and intestinal-intrinsic ILC2 expresses CCR4 but not CCR2. After IL-33/IL-25 stimulation: when intestinal ILC2s is stimulated by IL-25 it differentiates into iILC2; iILC2 relies on BATF and S1P for migration into the lung; Lung intrinsic ILC2 and iILC2 are activated by stimulation with IL-33 or IL-25. Returning tissue homeostasis: after the immune response subsides, some of the iILC2s transform into lung-intrinsic ILC2 and other parts of the ILC2s return to the small intestine through the circular system.