{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,1,16]],"date-time":"2026-01-16T07:14:47Z","timestamp":1768547687843,"version":"3.49.0"},"reference-count":68,"publisher":"Wiley","issue":"11","license":[{"start":{"date-parts":[[2004,10,21]],"date-time":"2004-10-21T00:00:00Z","timestamp":1098316800000},"content-version":"vor","delay-in-days":0,"URL":"http:\/\/onlinelibrary.wiley.com\/termsAndConditions#vor"}],"content-domain":{"domain":[],"crossmark-restriction":false},"short-container-title":["Experimental Dermatology"],"published-print":{"date-parts":[[2004,11]]},"abstract":"<jats:p><jats:bold>Abstract:\u2002<\/jats:bold> The angiogenic mediator vascular endothelial growth factor (VEGF) and its receptors (VEGFRs) have been studied extensively in neoplastic disease and some inflammatory conditions. Contact hypersensitivity (CHS) is a prototypic Langerhans' cell\u2010dependent, T\u2010helper (Th) 1 cell\u2010mediated inflammatory skin disease that is now also thought to involve angiogenic mediators. The purpose of our study was to examine the role of angiogenesis and VEGF in CHS. We demonstrated that VEGF production is up\u2010regulated in murine skin after challenge with dinitrofluorobenzene. Administration of a monoclonal antibody directed against the VEGFR\u20102 (DC101) resulted in a 28.8% decrease in CHS response (<jats:italic>P<\/jats:italic>\u2003&lt;\u20030.001). Examination of the DC101\u2010treated mouse skin 24\u2003h after challenge revealed decreases in dermal inflammatory cellular infiltrates and total vessel area. Furthermore, mRNA and protein of the Th1\u2010type cytokine interferon (IFN)\u2010\u03b3 was significantly down\u2010regulated in skin of DC101\u2010treated animals 24\u2003h after challenge. The results of the study demonstrate that VEGFR\u20102 blockade significantly reduces vascular enlargement and edema formation and effects IFN\u2010\u03b3 expression in the skin during challenge in CHS. Our findings suggest that DC101 could function by reducing inflammatory cell migration and hence IFN\u2010\u03b3 expression during the CHS response.<\/jats:p>","DOI":"10.1111\/j.0906-6705.2004.00240.x","type":"journal-article","created":{"date-parts":[[2004,10,21]],"date-time":"2004-10-21T14:02:31Z","timestamp":1098367351000},"page":"671-681","source":"Crossref","is-referenced-by-count":32,"title":["Anti\u2010vascular endothelial growth factor receptor\u20102 (Flk\u20101\/KDR) antibody suppresses contact hypersensitivity"],"prefix":"10.1111","volume":"13","author":[{"given":"Hideaki","family":"Watanabe","sequence":"first","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Adam J.","family":"Mamelak","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Binghe","family":"Wang","sequence":"additional","affiliation":[],"role":[{"role":"author","vocabulary":"crossref"}]},{"given":"Brandon 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