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However, the precise roles played by the IL-4\/IL-13 receptors and STAT6 in inducing AAM protein expression and modulating specific features of airway inflammation are still unclear. Since T<jats:sub>H<\/jats:sub>2 differentiation and activation plays a pivotal role in this disease, we explored the possibility of developing an asthma model in mice using T cells that were differentiated<jats:italic>in vivo<\/jats:italic>.<\/jats:p><\/jats:sec><jats:sec><jats:title>Results<\/jats:title><jats:p>In this study, we monitored the activation and proliferation status of adoptively transferred allergen-specific na\u00efve or<jats:italic>in vivo<\/jats:italic>primed CD4+ T cells. We found that both the na\u00efve and<jats:italic>in vivo<\/jats:italic>primed T cells expressed similar levels of CD44 and IL-4. However,<jats:italic>in vivo<\/jats:italic>primed T cells underwent reduced proliferation in a lymphopenic environment when compared to na\u00efve T cells. We then used these<jats:italic>in vivo<\/jats:italic>generated effector T cells in an asthma model. Although there was reduced inflammation in mice lacking IL-4R\u03b1 or STAT6, significant amounts of eosinophils were still present in the BAL and lung tissue. Moreover, specific AAM proteins YM1 and FIZZ1 were expressed by epithelial cells, while macrophages expressed only YM1 in RAG2<jats:sup>-\/-<\/jats:sup>mice. We further show that FIZZ1 and YM1 protein expression in the lung was completely dependent on signaling through the IL-4R\u03b1 and STAT6. Consistent with the enhanced inflammation and AAM protein expression, there was a significant increase in collagen deposition and smooth muscle thickening in RAG2<jats:sup>-\/-<\/jats:sup>mice compared to mice deficient in IL-4R\u03b1 or STAT6.<\/jats:p><\/jats:sec><jats:sec><jats:title>Conclusions<\/jats:title><jats:p>These results establish that transfer of<jats:italic>in vivo<\/jats:italic>primed CD4+ T cells can induce allergic lung inflammation. Furthermore, while IL-4\/IL-13 signaling through IL-4R\u03b1 and STAT6 is essential for AAM protein expression, lung inflammation and eosinophilia are only partially dependent on this pathway. Further studies are required to identify other proteins and signaling pathways involved in airway inflammation.<\/jats:p><\/jats:sec>","DOI":"10.1186\/1471-2172-12-60","type":"journal-article","created":{"date-parts":[[2011,11,9]],"date-time":"2011-11-09T20:29:05Z","timestamp":1320870545000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":28,"title":["Transfer of in vivo primed transgenic T cells supports allergic lung inflammation and FIZZ1 and Ym1 production in an IL-4R\u03b1 and STAT6 dependent manner"],"prefix":"10.1186","volume":"12","author":[{"given":"Preeta","family":"Dasgupta","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana P","family":"Chapoval","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth P","family":"Smith","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Achsah D","family":"Keegan","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2011,10,20]]},"reference":[{"key":"407_CR1","doi-asserted-by":"publisher","first-page":"939","DOI":"10.1084\/jem.187.6.939","volume":"187","author":"D Kuperman","year":"1998","unstructured":"Kuperman D, Schofield B, Wills-Karp M, Grusby MJ: Signal transducer and activator of transcription factor 6 (Stat6)-deficient mice are protected from antigen-induced airway hyperresponsiveness and mucus production. 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