{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,11,8]],"date-time":"2026-11-08T19:23:04Z","timestamp":1794165784080,"version":"4.8.0"},"reference-count":61,"publisher":"American Society for Clinical Investigation","issue":"21","license":[{"start":{"date-parts":[[2026,11,9]],"date-time":"2026-11-09T00:00:00Z","timestamp":1794182400000},"content-version":"vor","delay-in-days":48,"URL":"http:\/\/creativecommons.org\/licenses\/by\/4.0\/"}],"funder":[{"name":"National Institute of Environmental Health Sciences","award":["Z01 ES025034"],"award-info":[{"award-number":["Z01 ES025034"]}],"id":[{"id":"https:\/\/ror.org\/00j4k1h63","id-type":"ROR","asserted-by":"crossref"}]}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2026,11,9]]},"abstract":"<jats:p>\n                    Type 2 innate lymphoid cells (ILC2) are a population of lineage-negative cells in the lung, gastrointestinal tract, and skin that have emerged as a significant component of type 2 allergic inflammation. The regulation of cyclooxygenase-2 (COX-2) metabolites is critical to the pathophysiology of many inflammatory disorders, including allergic asthma. While COX-2 regulates Th9 and Th17 cell differentiation and function during allergic lung inflammation, it remains unknown whether COX-2 also regulates ILC2 cell differentiation and function under similar conditions. To address this question, we examined lung ILC2 cells from\n                    <jats:italic>\n                      COX-2\n                      <jats:sup>+\/+<\/jats:sup>\n                    <\/jats:italic>\n                    and\n                    <jats:italic>\n                      COX-2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    mice after ovalbumin-induced (OVA-induced) or\n                    <jats:italic>Alternaria<\/jats:italic>\n                    -induced allergic lung inflammation. ILC2 cells were significantly increased in\n                    <jats:italic>\n                      COX-2\n                      <jats:sup>\u2013\/\u2013<\/jats:sup>\n                    <\/jats:italic>\n                    lungs compared with\n                    <jats:italic>\n                      COX-2\n                      <jats:sup>+\/+<\/jats:sup>\n                    <\/jats:italic>\n                    lungs after OVA exposure in vivo. The increase in ILC2 cells was accompanied by an increase in expression of the cytokines IL-5 and IL-13 and of the transcription factor GATA3. Both genetic disruption and selective inhibition of COX-2 significantly increased ILC2 cell differentiation from isolated common lymphoid progenitor cells (CLP) in vitro. Furthermore, COX-2\u2013derived PGE\n                    <jats:sub>2<\/jats:sub>\n                    acting via EP2 receptors significantly reduced IL-33 and TSLP expression, and it attenuated ILC2 cell differentiation in vitro and in vivo. Thus, during allergic lung inflammation, COX-2\u2013derived PGE\n                    <jats:sub>2<\/jats:sub>\n                    signals through the EP2 receptor to negatively regulate lung ILC2 cell differentiation and function.\n                  <\/jats:p>","DOI":"10.1172\/jci.insight.189205","type":"journal-article","created":{"date-parts":[[2026,9,22]],"date-time":"2026-09-22T16:01:16Z","timestamp":1790092876000},"source":"Crossref","is-referenced-by-count":0,"title":["Cyclooxygenase-2 negatively regulates innate lymphoid cell type 2 differentiation and function during allergic lung inflammation"],"prefix":"10.1172","volume":"11","author":[{"given":"Hong","family":"Li","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"ORCID":"https:\/\/orcid.org\/0000-0002-7042-500X","authenticated-orcid":true,"given":"Matthew L.","family":"Edin","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Daniel","family":"Menendez","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"J. 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