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IL\u20104R\u03b1\u2010signaling is essential for driving T\n                      <jats:sub>H<\/jats:sub>\n                      2\u2010type immunity to allergens. Anti\u2010T\n                      <jats:sub>H<\/jats:sub>\n                      2 therapies have the potential to effectively reduce airway obstruction and inflammation in allergic asthma.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Objective<\/jats:title>\n                    <jats:p>We investigated potential therapeutic effects of selective inhibition of this pathway in mice with established allergic airway disease. We further investigated whether IL\u20104R\u03b1 disruption in systemically sensitized mice can prevent the onset of the disease.<\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Methods<\/jats:title>\n                    <jats:p>\n                      We used Rosa\n                      <jats:sup>creERT2<\/jats:sup>\n                      IL\u20104R\u03b1\n                      <jats:sup>\u2212\/lox<\/jats:sup>\n                      mice, a tamoxifen (TAM)\u2010inducible IL\u20104R\u03b1 knockdown model to investigate the role of IL\u20104\/IL\u201013 signaling prior to the onset of the disease and during the effector phase in the ovalbumin\u2010induced allergic airway disease.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Results<\/jats:title>\n                    <jats:p>\n                      Inducible deletion of IL\u20104R\u03b1 demonstrated therapeutic effects, on established allergic airway disease, and prevented the development of ovalbumin\u2010induced airway hyperreactivity, eosinophilia, and goblet cell metaplasia in allergen\u2010sensitized mice. Interestingly, IL\u20104R\u03b1 knockdown after allergic sensitization did not induce T\n                      <jats:sub>H<\/jats:sub>\n                      17, a neutrophilic inflammatory response as observed in global IL\u20104R\u03b1\u2010deficient mice after intranasal allergen challenge.\n                    <\/jats:p>\n                  <\/jats:sec>\n                  <jats:sec>\n                    <jats:title>Conclusion<\/jats:title>\n                    <jats:p>\n                      Abrogation of IL\u20104R\u03b1 signaling after allergic sensitization would have significant therapeutic benefit for T\n                      <jats:sub>H<\/jats:sub>\n                      2\u2010type allergic asthma.\n                    <\/jats:p>\n                  <\/jats:sec>","DOI":"10.1111\/all.14137","type":"journal-article","created":{"date-parts":[[2019,11,29]],"date-time":"2019-11-29T09:25:16Z","timestamp":1575019516000},"page":"1347-1360","update-policy":"https:\/\/doi.org\/10.1002\/crossmark_policy","source":"Crossref","is-referenced-by-count":11,"title":["Therapeutic and prophylactic deletion of IL\u20104Ra\u2010signaling ameliorates established ovalbumin induced allergic asthma"],"prefix":"10.1111","volume":"75","author":[{"given":"Jermaine","family":"Khumalo","sequence":"first","affiliation":[{"name":"Division of Immunology, and South African Medical Research Council (SAMRC) Immunology of Infectious Diseases Department of Pathology Faculty of Health Sciences University of Cape Town Cape Town South Africa"},{"name":"Division of Immunology Health Science Faculty International Centre for Genetic Engineering and Biotechnology (ICGEB) and Institute of Infectious Diseases and Molecular Medicine (IDM) University of Cape Town Cape Town South 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