title: Th2 cytokines, IgE and mast cells play a crucial role in the induction of para-phenylenediamine-induced contact hypersensitivity in mice.
abstract: We previously reported the establishment of a mouse model system of contact hypersensitivity (CHS) to paraphenylemediamine (PPD). In order to analyse the functional contribution of Th2 cytokines, IL-4 and IL-5, in PPD induced CHS, STAT6 deficient (STAT6-/-) and wild-type control (WT) mice (C57BL/6) were immunized by the topical application of a PPD solution, and then the subsequent skin reactions were examined. Ear swelling was significantly reduced with a delayed peak response in STAT6-/- mice as compared with that of WT mice. A histological analysis showed the infiltration of both eosinophils and neutrophils in the skin of STAT6-/- mice challenged 24 h previously to significantly decrease in comparison with that in the WT mice. The expression of Th2 cytokines (IL-4, IL-5) by ELISA in the PPD-challenged skin tissue specimens as well as the IgE and IgG1 response after challenge were also profoundly reduced in the STAT6-/- mice. The adoptive transfer of the serum obtained from sensitized WT mice for the putative IgE transfer induced a peak response at 3 h and 24 h after challenge. To further investigate the role of mast cells in the induction of PPD-CHS, mast cell deficient W/Wv mice were sensitized with PPD and then were challenged. Maximal ear swelling was detected from 12 to 24 h and another small peak response was observed at 1 h in+/+mice, whereas only a small peak response at 24 h was detected in W/Wv mice. These data indicate that not only Th2 cytokines and IgE but also mast cells play an essential role in the induction of PPD-CHS.
authors.affiliation: Department of Dermatology and Immunodermatology, Tokyo Medical and Dental University, Japan. 3064derm@tmd.ac.jp
authors.forename: H
authors.initials: H
authors.lastname: Yokozeki
authors.forename: M-H
authors.initials: MH
authors.lastname: Wu
authors.forename: K
authors.initials: K
authors.lastname: Sumi
authors.forename: K
authors.initials: K
authors.lastname: Igawa
authors.forename: Y
authors.initials: Y
authors.lastname: Miyazaki
authors.forename: I
authors.initials: I
authors.lastname: Katayama
authors.forename: K
authors.initials: K
authors.lastname: Takeda
authors.forename: S
authors.initials: S
authors.lastname: Akira
authors.forename: K
authors.initials: K
authors.lastname: Nishioka
mesh_terms: D019264:Adoptive Transfer; D000818:Animals; D016207:Cytokines / Q000276:immunology*; D003877:Dermatitis, Contact / Q000276:immunology* / Q000473:pathology; D005260:Female; D007073:Immunoglobulin E / Q000276:immunology*; D008407:Mast Cells / Q000276:immunology*; D051379:Mice; D008810:Mice, Inbred C57BL; D010655:Phenylenediamines; D050800:STAT6 Transcription Factor; D018418:Th2 Cells / Q000276:immunology*; D015534:Trans-Activators / Q000276:immunology; D014373:Tuberculin / Q000276:immunology
chemical_list: D016207:Cytokines; D010655:Phenylenediamines; D050800:STAT6 Transcription Factor; C494100:Stat6 protein, mouse; D015534:Trans-Activators; D014373:Tuberculin; D007073:Immunoglobulin E; C029728:4-phenylenediamine