{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T07:05:33Z","timestamp":1784099133427,"version":"3.55.0"},"reference-count":211,"publisher":"Frontiers Media SA","license":[{"start":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T00:00:00Z","timestamp":1784073600000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"content-domain":{"domain":["frontiersin.org"],"crossmark-restriction":true},"short-container-title":["Front. Immunol."],"abstract":"<jats:p>Respiratory diseases represent a major global public health burden, and type 2 immunity plays a key role in their pathogenesis. The interleukin-33 (IL-33)-group 2 innate lymphoid cell (ILC2) axis regulates airway type 2 immune responses, thereby triggering, amplifying, and maintaining pathological inflammation. This review addresses the characteristics of IL-33 and pulmonary ILC2s, including the alarmin function and tissue-specific expression of IL-33, and the origin, localization, functional heterogeneity, and microenvironment-driven plasticity of ILC2s. In particular, we discuss how disease-specific microenvironments shape divergent ILC2 states, including classical type 2 cytokine-producing ILC2s, tissue-repairing AREG-producing ILC2s, ILC1-like cells, and IL-17-producing ILC2-like states. We further review the regulatory mechanisms of the IL-33\u2013ILC2 axis in bronchopulmonary dysplasia, asthma, chronic obstructive pulmonary disease, pulmonary fibrosis, and viral respiratory infections are also discussed, highlighting the remarkable functional plasticity of ILC2s. Targeting the IL-33-ILC2 axis and modulating ILC2 function represent therapeutic strategies for various type 2-mediated airway diseases.<\/jats:p>","DOI":"10.3389\/fimmu.2026.1891857","type":"journal-article","created":{"date-parts":[[2026,7,15]],"date-time":"2026-07-15T06:10:01Z","timestamp":1784095801000},"update-policy":"https:\/\/doi.org\/10.3389\/crossmark-policy","source":"Crossref","is-referenced-by-count":0,"title":["The IL-33-ILC2 axis: a key regulator of type 2 immunity in respiratory disease"],"prefix":"10.3389","volume":"17","author":[{"given":"Yue","family":"Zhu","sequence":"first","affiliation":[{"name":"Department of Neonatal Medical Center, Children\u2019s Hospital of Nanjing Medical University","place":["Nanjing, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Yi","family":"Zhang","sequence":"additional","affiliation":[{"name":"Department of Applied Physics, The Hong Kong Polytechnic University","place":["Hong Kong, Hong Kong SAR, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Rui","family":"Cheng","sequence":"additional","affiliation":[{"name":"Department of Neonatal Medical Center, Children\u2019s Hospital of Nanjing Medical University","place":["Nanjing, Jiangsu, China"]}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"1965","published-online":{"date-parts":[[2026,7,15]]},"reference":[{"key":"B1","doi-asserted-by":"publisher","DOI":"10.1038\/s41423-025-01261-2","article-title":"Type 2 immunity in allergic diseases","volume":"22","author":"Ogulur","year":"2025","journal-title":"Cell Mol Immunol"},{"key":"B2","doi-asserted-by":"publisher","DOI":"10.1111\/imr.12557","article-title":"Innate and adaptive type 2 immunity in lung allergic inflammation","volume":"278","author":"Kubo","year":"2017","journal-title":"Immunol Rev"},{"key":"B3","doi-asserted-by":"publisher","DOI":"10.1016\/j.jaci.2024.11.003","article-title":"Update on type 2 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