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Notably, we consider the complexity of type\u20102 responses and studies that have explored integrated signaling among classical\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    2 cytokines (\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20104,\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u20105, and\n                    <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\n                    \u201013), which together with\n                    <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>\n                    11 (eotaxin\u20101) regulate critical aspects of eosinophil recruitment, allergic inflammation, and airway hyper\u2010responsiveness (\n                    <jats:styled-content style=\"fixed-case\">AHR<\/jats:styled-content>\n                    ). Among our most important findings, we have provided evidence that the initiation of\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    2 responses is regulated by airway epithelial cell\u2010derived factors, including\n                    <jats:styled-content style=\"fixed-case\">TRAIL<\/jats:styled-content>\n                    and\n                    <jats:styled-content style=\"fixed-case\">MID<\/jats:styled-content>\n                    1, which promote\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    2 cell development via\n                    <jats:styled-content style=\"fixed-case\">STAT<\/jats:styled-content>\n                    6\u2010dependent pathways. Further, we highlight studies demonstrating that micro\n                    <jats:styled-content style=\"fixed-case\">RNAs<\/jats:styled-content>\n                    are key regulators of allergic inflammation and potential targets for anti\u2010inflammatory therapy. On the background of\n                    <jats:styled-content style=\"fixed-case\">\n                      T\n                      <jats:sub>H<\/jats:sub>\n                    <\/jats:styled-content>\n                    2 inflammation, we have demonstrated that innate immune cells (notably, airway macrophages) play essential roles in the generation of steroid\u2010resistant inflammation and\n                    <jats:styled-content style=\"fixed-case\">AHR<\/jats:styled-content>\n                    secondary to allergen\u2010 and pathogen\u2010induced exacerbations. Our work clearly indicates that understanding the diversity and spatiotemporal role of the inflammatory response and its interactions with resident airway cells is critical to advancing knowledge on asthma pathogenesis and the development of new therapeutic approaches.\n                  <\/jats:p>","DOI":"10.1111\/imr.12549","type":"journal-article","created":{"date-parts":[[2017,6,28]],"date-time":"2017-06-28T13:15:22Z","timestamp":1498655722000},"page":"20-40","source":"Crossref","is-referenced-by-count":125,"title":["Modeling\n                    <scp>\n                      T\n                      <sub>H<\/sub>\n                    <\/scp>\n                    2 responses and airway inflammation to understand fundamental mechanisms regulating the pathogenesis of asthma"],"prefix":"10.1111","volume":"278","author":[{"ORCID":"https:\/\/orcid.org\/0000-0002-0827-8299","authenticated-orcid":false,"given":"Paul S.","family":"Foster","sequence":"first","affiliation":[{"name":"Priority 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