{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,5,30]],"date-time":"2026-05-30T12:02:43Z","timestamp":1780142563652,"version":"3.54.0"},"reference-count":77,"publisher":"Oxford University Press (OUP)","issue":"4","license":[{"start":{"date-parts":[[2013,8,1]],"date-time":"2013-08-01T00:00:00Z","timestamp":1375315200000},"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":[[2013,8,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>STAT6 plays a central role in IL-4\u2013mediated allergic responses. Several studies indicate that regulatory T cells (Tregs) can be modulated by IL-4 in vitro. We previously showed that STAT6\u2212\/\u2212 mice are highly resistant to allergic lung inflammation even when wild-type Th2 effectors were provided and that they have increased numbers of Tregs. However, the role of STAT6 in modulating Tregs in vivo during allergic lung inflammation has not been thoroughly investigated. To examine Treg and STAT6 interaction during allergic inflammation, STAT6\u2212\/\u2212, STAT6xRAG2\u2212\/\u2212, and RAG2\u2212\/\u2212 mice were subjected to OVA sensitization and challenge following adoptive transfer of OVA-specific, wild-type Th2 effectors with or without prior Treg depletion\/inactivation, using anti-CD25 (PC61). As expected, STAT6\u2212\/\u2212 mice were highly resistant to airway inflammation and remodeling. In contrast, allergic lung inflammation was partially restored in STAT6\u2212\/\u2212 mice treated with PC61 to levels observed in STAT6xRAG2\u2212\/\u2212 mice. In some cases, STAT6xRAG2\u2212\/\u2212 mice were also given natural Tregs along with Th2 effectors. Adoptive transfer of natural Tregs caused a substantial reduction in bronchoalveolar lavage eosinophil composition and suppressed airway remodeling and T cell migration into the lung in STAT6xRAG2\u2212\/\u2212 mice to levels comparable to those in STAT6\u2212\/\u2212 mice. These results demonstrate the STAT6-dependent suppression of Tregs in vivo to promote allergic airway inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.1300486","type":"journal-article","created":{"date-parts":[[2013,7,4]],"date-time":"2013-07-04T08:25:30Z","timestamp":1372926330000},"page":"1517-1528","source":"Crossref","is-referenced-by-count":25,"title":["STAT6 Controls the Number of Regulatory T Cells In Vivo, Thereby Regulating Allergic Lung Inflammation"],"prefix":"10.1093","volume":"191","author":[{"given":"Nicolas J","family":"Dorsey","sequence":"first","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Svetlana P","family":"Chapoval","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Program in Oncology, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Elizabeth P","family":"Smith","sequence":"additional","affiliation":[{"name":"Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jonathan","family":"Skupsky","sequence":"additional","affiliation":[{"name":"Department of Internal Medicine, University of California\u2013Irvine , Orange, CA 92604"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W","family":"Scott","sequence":"additional","affiliation":[{"name":"Department of Medicine, Uniformed Services University of Health Sciences , Bethesda, MD 20814"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Achsah D","family":"Keegan","sequence":"additional","affiliation":[{"name":"Department of Microbiology and Immunology, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Center for Vascular and Inflammatory Diseases, University of Maryland School of Medicine , Baltimore, MD 21201"},{"name":"Program in Oncology, Marlene and Stewart Greenebaum Cancer Center, University of Maryland School of Medicine , Baltimore, MD 21201"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2013,8,15]]},"reference":[{"key":"2025032405171327600_r1","doi-asserted-by":"crossref","first-page":"777","DOI":"10.1016\/j.cell.2010.03.004","article-title":"Asthma and allergic inflammation","volume":"140","author":"Locksley","year":"2010","journal-title":"Cell"},{"key":"2025032405171327600_r2","doi-asserted-by":"crossref","first-page":"410","DOI":"10.1016\/j.jaci.2006.06.004","article-title":"IL-4 induces IL-13-independent allergic airway inflammation","volume":"118","author":"Perkins","year":"2006","journal-title":"J. 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