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Here we show the involvement of AQP9 in hapten-induced contact hypersensitivity (CHS), as a murine model of skin allergic contact dermatitis, using AQP9 knockout (AQP9<jats:sup>\u2212\/\u2212<\/jats:sup>) mice. First, the CHS response to hapten dinitrofluorobenzene (DNFB) was impaired in AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> mice compared with wild-type (WT) mice. Adoptive transfer of sensitized AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> draining lymph node (dLN) cells into WT recipients resulted in a reduced CHS response, indicating impaired sensitization in AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> mice. Second, administration of WT neutrophils into AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> mice during sensitization rescued the impaired CHS response. Neutrophil recruitment to dLNs upon hapten application was attenuated by AQP9 deficiency. Coincidentally, AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> neutrophils showed a reduced CC-chemokine receptor 7 (CCR7) ligand-induced migration efficacy, which was attributed to the attenuated recruitment of neutrophils to dLNs. Furthermore, we found that neutrophil deficiency, observed in AQP9<jats:sup>\u2212\/\u2212<\/jats:sup> or neutrophil-depleted mice, decreased IL-17A production by dLN cells, which might be responsible for T cell activation during a subsequent CHS response. Taken together, these findings suggest that AQP9 is required for the development of sensitization during cutaneous acquired immune responses via regulating neutrophil function.<\/jats:p>","DOI":"10.1038\/srep15319","type":"journal-article","created":{"date-parts":[[2015,10,22]],"date-time":"2015-10-22T09:15:42Z","timestamp":1445505342000},"update-policy":"https:\/\/doi.org\/10.1007\/springer_crossmark_policy","source":"Crossref","is-referenced-by-count":48,"title":["Aquaporin-9-expressing neutrophils are required for the establishment of contact hypersensitivity"],"prefix":"10.1038","volume":"5","author":[{"given":"Catharina Sagita","family":"Moniaga","sequence":"first","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Sachiko","family":"Watanabe","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Tetsuya","family":"Honda","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"S\u00f8ren","family":"Nielsen","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Mariko","family":"Hara-Chikuma","sequence":"additional","affiliation":[],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"297","published-online":{"date-parts":[[2015,10,22]]},"reference":[{"key":"BFsrep15319_CR1","doi-asserted-by":"publisher","first-page":"1","DOI":"10.1111\/j.1600-0463.2011.02832.x","volume":"120","author":"AD Christensen","year":"2012","unstructured":"Christensen, A. D. & Haase, C. Immunological mechanisms of contact hypersensitivity in mice. APMIS: acta pathologica, microbiologica, et immunologica Scandinavica 120, 1\u201327, 10.1111\/j.1600-0463.2011.02832.x (2012).","journal-title":"APMIS: acta pathologica, microbiologica, et immunologica Scandinavica"},{"key":"BFsrep15319_CR2","doi-asserted-by":"publisher","first-page":"303","DOI":"10.1038\/jid.2012.284","volume":"133","author":"T Honda","year":"2013","unstructured":"Honda, T., Egawa, G., Grabbe, S. & Kabashima, K. Update of immune events in the murine contact hypersensitivity model: toward the understanding of allergic contact dermatitis. The Journal of investigative dermatology 133, 303\u2013315, 10.1038\/jid.2012.284 (2013).","journal-title":"The Journal of investigative dermatology"},{"key":"BFsrep15319_CR3","doi-asserted-by":"publisher","first-page":"1154","DOI":"10.1016\/j.jaci.2009.12.005","volume":"125","author":"T Honda","year":"2010","unstructured":"Honda, T. et al. 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