{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,7,30]],"date-time":"2026-07-30T12:59:17Z","timestamp":1785416357081,"version":"3.56.0"},"reference-count":34,"publisher":"Wiley","issue":"5","license":[{"start":{"date-parts":[[2012,4,26]],"date-time":"2012-04-26T00:00:00Z","timestamp":1335398400000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"funder":[{"name":"See accompanying article by Costa et al."}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Eur J Immunol"],"published-print":{"date-parts":[[2012,5]]},"abstract":"<jats:p>Chemokines are traditionally classified as homeostatic or inflammatory depending on whether they direct leukocyte migration in the absence or presence of inflammatory stimuli. CC chemokine ligand (CCL)25, a ligand for CC chemokine receptor (CCR)9, has mostly been characterized as a homeostatic chemokine that determines the migration pathway of <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell progenitors within the thymus, and the recruitment of various lymphocyte subsets to the intestinal mucosa. In this issue of the <jats:italic>European Journal of Immunology<\/jats:italic>, Costa et al. [Eur. J. Immunol. 2012. 42: 1250\u20131260] describe a new inflammatory role for <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>25\/<jats:styled-content style=\"fixed-case\">CCR<\/jats:styled-content>9 in controlling the migration of a subset of \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>cells committed to <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 production (\u03b3\u03b417 cells) in a model of allergic pleurisy. Interestingly, the effect of <jats:styled-content style=\"fixed-case\">CCL<\/jats:styled-content>25 was selective for \u03b3\u03b417 cells, as it did not extend to other \u03b3\u03b4 or \u03b1\u03b2 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>\u2010cell subsets, and resulted in a specific increase of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 (but not <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u20104 or <jats:styled-content style=\"fixed-case\">IFN<\/jats:styled-content>\u2010\u03b3) levels in the allergic pleura. In this commentary<jats:italic>,<\/jats:italic> I discuss these results in the context of chemokine\u2010mediated recruitment of \u03b3\u03b4 <jats:styled-content style=\"fixed-case\">T<\/jats:styled-content>cells to inflammatory sites, and the as yet unclear and controversial role of <jats:styled-content style=\"fixed-case\">IL<\/jats:styled-content>\u201017 in allergic reactions.<\/jats:p>","DOI":"10.1002\/eji.201242545","type":"journal-article","created":{"date-parts":[[2012,4,26]],"date-time":"2012-04-26T18:49:03Z","timestamp":1335466143000},"page":"1097-1101","source":"Crossref","is-referenced-by-count":7,"title":["Driving <scp>IL<\/scp>\u201017<sup>+<\/sup> \u03b3\u03b4 <scp>T<\/scp>\u2010cell migration in allergic reactions: A new \u201cinflammatory\u201d role for the \u201chomeostatic\u201d chemokine <scp>CCL<\/scp>25"],"prefix":"10.1002","volume":"42","author":[{"given":"Bruno","family":"Silva\u2010Santos","sequence":"first","affiliation":[{"name":"Instituto de Medicina Molecular Faculdade de Medicina da Universidade de Lisboa Lisboa Portugal"},{"name":"Instituto Gulbenkian de Ci\u00eancia Oeiras 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