{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,25]],"date-time":"2026-09-25T23:49:55Z","timestamp":1790380195004,"version":"4.1.0"},"reference-count":66,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2006,12,1]],"date-time":"2006-12-01T00:00:00Z","timestamp":1164931200000},"content-version":"vor","delay-in-days":0,"URL":"https:\/\/academic.oup.com\/pages\/standard-publication-reuse-rights"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":[],"published-print":{"date-parts":[[2006,12,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n                  <jats:sec>\n                    <jats:title>Rationale<\/jats:title>\n                    <jats:p>Nuclear receptors play a critical role in the regulation of inflammation, thus representing attractive targets for the treatment of asthma.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>In this study, we assess the potential regulatory function of retinoid-related orphan receptor \u03b1 (ROR\u03b1) in the adaptive immune response using ovalbumin (OVA)-induced airway inflammation as a model.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>Allergen-induced inflammation was compared between wild-type (WT) and staggerer (ROR\u03b1sg\/sg) mice, a natural mutant strain that is deficient in ROR\u03b1 expression.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Measurements and Main Results<\/jats:title>\n                    <jats:p>Despite robust increases in OVA-specific IgE, ROR\u03b1sg\/sg mice developed significantly less pulmonary inflammation, mucous cell hyperplasia, and eosinophilia compared with similarly treated WT animals. Induction of Th2 cytokines, including interleukin (IL)-4, IL-5, and IL-13, was also significantly less in ROR\u03b1sg\/sg mice. Microarray analysis using lung RNA showed increased expression of many genes, previously implicated in inflammation, in OVA-treated WT mice. These include mucin Muc5b, the chloride channel calcium-activated 3 (Clca3), macrophage inflammatory protein (MIP) 1\u03b1 and 1\u03b2, eotaxin-2, serum amyloid A3 (Saa3), and insulin-like growth factor 1 (Igf1). These genes were induced to a greater extent in OVA-treated WT mice relative to ROR\u03b1sg\/sg mice.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusions<\/jats:title>\n                    <jats:p>Our study demonstrates that mice deficient in ROR\u03b1 exhibit an attenuated allergic inflammatory response, indicating that ROR\u03b1 plays a critical role in the development of Th2-driven allergic lung inflammation in mice, and suggests that this nuclear receptor should be further evaluated as a potential asthma target.<\/jats:p>\n                  <\/jats:sec>","DOI":"10.1164\/rccm.200510-1672oc","type":"journal-article","created":{"date-parts":[[2006,9,14]],"date-time":"2006-09-14T21:36:42Z","timestamp":1158269802000},"page":"1299-1309","source":"Crossref","is-referenced-by-count":71,"title":["Modulatory Role for Retinoid-related Orphan Receptor \u03b1 in Allergen-induced Lung Inflammation"],"prefix":"10.1093","volume":"174","author":[{"given":"Maisa","family":"Jaradat","sequence":"first","affiliation":[{"name":"Cell Biology Section, Laboratory of Respiratory Biology, and Microarray Group, Laboratory of Experimental Pathology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park; and Pulmonary Immunobiology Laboratory, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Cliona","family":"Stapleton","sequence":"additional","affiliation":[{"name":"Cell Biology Section, Laboratory of Respiratory Biology, and Microarray Group, Laboratory of Experimental Pathology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park; and Pulmonary Immunobiology 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G.","family":"McCaskill","sequence":"additional","affiliation":[{"name":"Cell Biology Section, Laboratory of Respiratory Biology, and Microarray Group, Laboratory of Experimental Pathology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park; and Pulmonary Immunobiology Laboratory, Division of Pulmonary and Critical Care Medicine, Department of Medicine, University of North Carolina, Chapel Hill, North Carolina"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Hong Soon","family":"Kang","sequence":"additional","affiliation":[{"name":"Cell Biology Section, Laboratory of Respiratory Biology, and Microarray Group, Laboratory of Experimental Pathology, Division of Intramural Research, National Institute of Environmental Health Sciences, National Institutes of Health, Research Triangle Park; and Pulmonary Immunobiology Laboratory, Division of Pulmonary and Critical Care Medicine, 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