{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,3,21]],"date-time":"2026-03-21T20:39:34Z","timestamp":1774125574375,"version":"3.50.1"},"reference-count":45,"publisher":"Wiley","issue":"8","license":[{"start":{"date-parts":[[2004,8,4]],"date-time":"2004-08-04T00:00:00Z","timestamp":1091577600000},"content-version":"vor","delay-in-days":3,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2004,8]]},"abstract":"<jats:title>Summary<\/jats:title><jats:p><jats:bold>Background\n\t\t\t\t\t<\/jats:bold> Allergen\u2010induced sensitization and airway disease are the results of adverse immune reactions against environmental antigens that may be prevented or inhibited by immune modifying strategies.<\/jats:p><jats:p><jats:bold>Objective\n\t\t\t\t\t<\/jats:bold> To investigate the effects of the novel immune response modifier resiquimod (R\u2010848), from the family of imidazol\u2010derivates, in a murine model of allergen\u2010mediated Th2\u2010immune responses and concomitant airway inflammation and airway hyper\u2010reactivity.<\/jats:p><jats:p><jats:bold>Methods\n\t\t\t\t\t<\/jats:bold> BALB\/c mice were systemically sensitized with ovalbumin (OVA) on days 1 and 14 and challenged with OVA aerosol on days 28 and 29. R\u2010848 was applied intranasally to sensitized animals once prior to the first allergen airway challenge, on day 27.<\/jats:p><jats:p><jats:bold>Results\n\t\t\t\t\t<\/jats:bold> A single application of R\u2010848 significantly reduced numbers of eosinophils and lymphocytes in bronchoalveolar lavage fluid and inhibited mucus gland hyperplasia, compared with sensitized and challenged controls. Associated with the decrease in airway inflammation, single intranasal treatment with R\u2010848 abolished the development of airway hyper\u2010reactivity after allergen sensitization and airway challenges. Additionally, Th2\u2010cytokine production in lung tissues from sensitized and R\u2010848\u2010treated animals was reduced, whereas IL\u201012 and IFN\u2010\u03b3 production was increased, compared with non\u2010treated sensitized mice.<\/jats:p><jats:p><jats:bold>Conclusion\n\t\t\t\t\t<\/jats:bold> These data indicate that R\u2010848 effectively inhibits allergen\u2010induced airway inflammation and hyper\u2010reactivity by modulation of increased Th2\u2010immune responses.<\/jats:p>","DOI":"10.1111\/j.1365-2222.2004.02023.x","type":"journal-article","created":{"date-parts":[[2004,8,4]],"date-time":"2004-08-04T14:31:29Z","timestamp":1091629889000},"page":"1314-1320","source":"Crossref","is-referenced-by-count":54,"title":["Resiquimod, a new immune response modifier from the family of imidazoquinolinamines, inhibits allergen\u2010induced Th2 responses, airway inflammation and airway hyper\u2010reactivity in 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