{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,3]],"date-time":"2026-10-03T22:28:45Z","timestamp":1791066525560,"version":"4.1.0"},"reference-count":43,"publisher":"Wiley","issue":"2","license":[{"start":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T00:00:00Z","timestamp":1314835200000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Clin Experimental Allergy"],"published-print":{"date-parts":[[2012,2]]},"abstract":"Summary<\/jats:title>Background<\/jats:title>The chemokine receptor CCR<\/jats:styled-content>4 has been implicated in Th<\/jats:styled-content>2 cell\u2010mediated immune responses. However, other T<\/jats:styled-content> cell subsets are also known to participate in allergic inflammation.<\/jats:p><\/jats:sec>Objective<\/jats:title>The role of CCR<\/jats:styled-content>4 in Th<\/jats:styled-content>1, Th<\/jats:styled-content>2, and Th<\/jats:styled-content>17 cell\u2010mediated allergic airway inflammation was investigated.<\/jats:p><\/jats:sec>Method<\/jats:title>We generated an allergic airway inflammation model by adoptive transfer of in vitro<\/jats:italic>\u2010polarized ovalbumin (OVA<\/jats:styled-content>)\u2010specific Th<\/jats:styled-content>1, Th<\/jats:styled-content>2, and Th<\/jats:styled-content>17 cells. The effect of a low\u2010molecular weight CCR<\/jats:styled-content>4 antagonist, C<\/jats:styled-content>ompound 22, on this model was examined.<\/jats:p><\/jats:sec>Results<\/jats:title>Upon in vitro<\/jats:italic> polarization of DO<\/jats:styled-content>11.10 na\u00efve T<\/jats:styled-content> cells, Th<\/jats:styled-content>1\u2010 and Th<\/jats:styled-content>2\u2010polarized cells dominantly expressed CXCR<\/jats:styled-content>3 and CCR<\/jats:styled-content>4, respectively, while Th<\/jats:styled-content>17\u2010polarized cells expressed CCR<\/jats:styled-content>6 and CCR<\/jats:styled-content>4. Intranasal OVA<\/jats:styled-content>\u2010challenge of mice transferred with each T<\/jats:styled-content> cell subset induced accumulation of T<\/jats:styled-content> cells in the lungs. Eosinophils were also massively accumulated in Th<\/jats:styled-content>2\u2010transferred mice, whereas neutrophils were preferentially recruited in Th<\/jats:styled-content>1\u2010 and Th<\/jats:styled-content>17\u2010transferred mice. C<\/jats:styled-content>ompound 22, as well as anti\u2010CCL<\/jats:styled-content>17 or anti\u2010CCL<\/jats:styled-content>22 antibody selectively suppressed accumulation of Th<\/jats:styled-content>2 cells and eosinophils in the lungs of Th<\/jats:styled-content>2\u2010transferred and OVA<\/jats:styled-content>\u2010challenged mice. C<\/jats:styled-content>ompound 22 also inhibited bronchial hyperresponsiveness but had little effect on goblet cell hyperplasia in Th<\/jats:styled-content>2\u2010transferred and OVA<\/jats:styled-content>\u2010challenged mice.<\/jats:p><\/jats:sec>Conclusions and Clinical Relevance<\/jats:title>There were notable differences in allergic lung inflammation mediated by different T<\/jats:styled-content> cell subsets. CCR<\/jats:styled-content>4 blockage was selectively effective for suppression of Th<\/jats:styled-content>2\u2010mediated allergic inflammation by blocking infiltration of Th<\/jats:styled-content>2 cells.<\/jats:p><\/jats:sec>","DOI":"10.1111\/j.1365-2222.2011.03847.x","type":"journal-article","created":{"date-parts":[[2011,9,1]],"date-time":"2011-09-01T18:31:23Z","timestamp":1314901883000},"page":"315-325","source":"Crossref","is-referenced-by-count":33,"title":["Selective down\u2010regulation of Th<\/scp>2 cell\u2010mediated airway inflammation in mice by pharmacological intervention of CCR<\/scp>4"],"prefix":"10.1111","volume":"42","author":[{"given":"O.","family":"Kaminuma","sequence":"first","affiliation":[{"name":"Department of Allergy and Immunology The Tokyo Metropolitan Institute of Medical Science Tokyo Japan"},{"name":"Clinical Research Center for Allergy and Rheumatology National Hospital Organization Sagamihara National Hospital Kanagawa 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