{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,29]],"date-time":"2026-07-29T00:19:45Z","timestamp":1785284385167,"version":"3.55.0"},"reference-count":40,"publisher":"Oxford University Press (OUP)","issue":"12","license":[{"start":{"date-parts":[[2012,6,1]],"date-time":"2012-06-01T00:00:00Z","timestamp":1338508800000},"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":[[2012,6,15]]},"abstract":"<jats:title>Abstract<\/jats:title>\n               <jats:p>The regulators of G protein signaling (RGS) protein superfamily negatively controls G protein-coupled receptor signal transduction pathways. RGS16 is enriched in activated\/effector T lymphocytes. In this paper, we show that RGS16 constrains pulmonary inflammation by regulating chemokine-induced T cell trafficking in response to challenge with Schistosoma mansoni. Naive Rgs16\u2212\/\u2212 mice were \u201cprimed\u201d for inflammation by accumulation of CCR10+ T cells in the lung. Upon pathogen exposure, these mice developed more robust granulomatous lung fibrosis than wild-type counterparts. Distinct Th2 or putative Th17 subsets expressing CCR4 or CCR10 accumulated more rapidly in Rgs16\u2212\/\u2212 lungs following challenge and produced proinflammatory cytokines IL-13 and IL-17B. CCR4+Rgs16\u2212\/\u2212 Th2 cells migrated excessively to CCL17 and localized aberrantly in challenged lungs. T lymphocytes were partially excluded from lung granulomas in Rgs16\u2212\/\u2212 mice, instead forming peribronchial\/perivascular aggregates. Thus, RGS16-mediated confinement of T cells to Schistosome granulomas mitigates widespread cytokine-mediated pulmonary inflammation.<\/jats:p>","DOI":"10.4049\/jimmunol.1103781","type":"journal-article","created":{"date-parts":[[2012,5,17]],"date-time":"2012-05-17T17:07:33Z","timestamp":1337274453000},"page":"6347-6356","source":"Crossref","is-referenced-by-count":37,"title":["RGS16 Attenuates Pulmonary Th2\/Th17 Inflammatory Responses"],"prefix":"10.1093","volume":"188","author":[{"given":"Sucharita P","family":"Shankar","sequence":"first","affiliation":[{"name":"Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mark S","family":"Wilson","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jeffrey A","family":"DiVietro","sequence":"additional","affiliation":[{"name":"Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Margaret M","family":"Mentink-Kane","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Zhihui","family":"Xie","sequence":"additional","affiliation":[{"name":"Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Thomas A","family":"Wynn","sequence":"additional","affiliation":[{"name":"Immunopathogenesis Section, Laboratory of Parasitic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Kirk M","family":"Druey","sequence":"additional","affiliation":[{"name":"Molecular Signal Transduction Section, Laboratory of Allergic Diseases, National Institute of Allergy and Infectious Diseases, National Institutes of Health , Bethesda, MD 20892"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"286","published-online":{"date-parts":[[2012,6,15]]},"reference":[{"key":"2025032410162012200_r1","doi-asserted-by":"crossref","first-page":"5","DOI":"10.1034\/j.1600-065X.2003.00075.x","article-title":"Lymphoid organ development and cell migration","volume":"195","author":"Cyster","year":"2003","journal-title":"Immunol. 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