{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T07:02:58Z","timestamp":1790060578507,"version":"4.0.1"},"reference-count":62,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T00:00:00Z","timestamp":1787529600000},"content-version":"vor","delay-in-days":23,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"},{"start":{"date-parts":[[2026,8,1]],"date-time":"2026-08-01T00:00:00Z","timestamp":1785542400000},"content-version":"tdm","delay-in-days":0,"URL":"http:\/\/doi.wiley.com\/10.1002\/tdm_license_1.1"}],"content-domain":{"domain":["onlinelibrary.wiley.com"],"crossmark-restriction":true},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2026,8]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Interleukin\u20109 (IL\u20109) has primarily been associated with type 2 immunity in health and disease. While its impact on innate lymphoid cells (ILC2s) is well known, the cellular targets and mechanisms underlying type 2 immunity remain incompletely understood. In this study, we report the generation of a mouse\u2010specific anti\u2010IL\u20109 receptor (IL\u20109R) antibody, enabling us to accurately map IL\u20109R protein expression across various immune cell types. In na\u00efve mice, IL\u20109R was detectable in ILC2s, marginal zone B cells, and B1b cells. In allergic lung inflammation, a subset of CD4\n                    <jats:sup>+<\/jats:sup>\n                    T cells faintly upregulated IL\u20109R, whereas DCs, macrophages, eosinophils, and neutrophils remained IL\u20109R\u2010negative. Functionally, IL\u20109R was found to significantly contribute to ILC2 expansion, their effector cytokine production, and eosinophilia in the papain asthma model. However, in the context of acute and chronic HDM exposure, IL\u20109R was dispensable for both allergic lung inflammation and CD4\u2010dependent memory\u2010type 2 responses. Using mixed bone marrow chimeras in which IL\u20109R is selectively absent in T cells, we confirmed that IL\u20109R signaling in T cells does not critically impact chronic Th2 and Th17 responses. Lastly, using mice selectively lacking ILC2s, we demonstrate that this population is the culprit of pathological type 2 immunity in the lung in both papain\u2010 and acute HDM\u2010induced asthma models. Together, our results establish that IL\u20109 is a critical regulator of ILC2\u2010dependent type 2 immunity, while its effects on T cell\u2010dependent responses are minimal. These findings provide a foundation for future studies exploring the therapeutic modulation of IL\u20109 signaling in allergy and other inflammatory diseases.\n                  <\/jats:p>","DOI":"10.1002\/eji.70270","type":"journal-article","created":{"date-parts":[[2026,8,24]],"date-time":"2026-08-24T12:52:45Z","timestamp":1787575965000},"update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":0,"title":["IL\u20109 Is Essential for ILC2\u2010Mediated but Not Th2\u2010 and Th17\u2010Cell\u2010Mediated Allergic Airway Inflammation in Mice"],"prefix":"10.1002","volume":"56","author":[{"ORCID":"https:\/\/orcid.org\/0000-0003-3257-3455","authenticated-orcid":false,"given":"Nikolaos D.","family":"Sidiropoulos","sequence":"first","affiliation":[{"name":"Institute of Molecular Health Sciences ETH Z\u00fcrich  Z\u00fcrich Switzerland"},{"name":"Institute of Physiology University of Z\u00fcrich  Z\u00fcrich 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Switzerland"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-0628-7140","authenticated-orcid":false,"given":"Manfred","family":"Kopf","sequence":"additional","affiliation":[{"name":"Institute of Molecular Health Sciences ETH Z\u00fcrich  Z\u00fcrich 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