| http://purl.uniprot.org/citations/15096484 | http://www.w3.org/1999/02/22-rdf-syntax-ns#type | http://purl.uniprot.org/core/Journal_Citation |
| http://purl.uniprot.org/citations/15096484 | http://www.w3.org/2000/01/rdf-schema#comment | "Contact hypersensitivity (CHS) induced by a hapten is thought to be mediated by T helper type 1 (Th1) cells. However, FITC can induce contact allergy in vivo, and in vitro studies suggest that this response is Th2-type driven. We compared CHS reactions induced by FITC or dinitrofluorobenzene (DNFB), a well-known Th1 inducing hapten, in Balb/c mice, C57/B6 mice, and several gene knock-out mice, and investigated the role of Th1/Th2 cytokines, T cell populations, eosinophils, and mast cells. Balb/c mice (Th2 dominant strain) had a stronger response to FITC than C57/B6 mice (Th1 dominant strain). The skin inflammation was characterized by edema and eosinophilia, and serum IgE levels were elevated following FITC challenge. All responses were enhanced by a second round of sensitization. Anti-TNF-alpha or anti-very late antigen-4 (VLA-4) antibody partly inhibited both FITC- and DNFB-induced CHS. Pretreatment of mice with anti-IL-4 antibody, anti-IL-5 antibody, recombinant INF-gamma, or the mast-cell depleting agent 48/80 significantly diminished edema formation, and Stat6(-/-) mice were fully protected from FITC-induced CHS, while DNFB-induced CHS was enhanced (Stat6(-/-), mast cell depletion) or not affected (anti-IL-5 antibody). Further, mice lacking CD4(+) T cells and mice lacking both CD8 and MHC II showed very little reaction at all to FITC, while the absence of CD8 T cells alone or MHC II alone conferred partial protection only. These findings indicate a contribution of MHC II-independent CD4(+) T cells and/or CD4(+) NKT cells to the Th2 response triggered by FITC in vivo, and makes FITC-induced CHS a suitable animal model for atopic dermatitis."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.org/dc/terms/identifier | "doi:10.1093/intimm/dxh073"xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/author | "Yamasaki T."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/author | "Akira S."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/author | "Takeshita K."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/author | "Bacon K.B."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/author | "Gantner F."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/date | "2004"xsd:gYear |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/name | "Int Immunol"xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/pages | "685-695"xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/title | "Essential role of MHC II-independent CD4+ T cells, IL-4 and STAT6 in contact hypersensitivity induced by fluorescein isothiocyanate in the mouse."xsd:string |
| http://purl.uniprot.org/citations/15096484 | http://purl.uniprot.org/core/volume | "16"xsd:string |
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