title: Spontaneous hair follicle cycling may influence the development of murine contact photosensitivity by modulating keratinocyte cytokine production.
abstract: The development of murine contact hypersensitivity is influenced by hair follicle cycling. Here, we have examined hair cycle-associated fluctuations of murine contact photosensitivity (CPS) to tetrachlorosalicylanilide (TCSA) and its immunologic mechanism(s). When the CPS outcome was monitored in correlation with their spontaneous, synchronized hair cycling, mice aged 8 and 14 weeks, with most of their hair follicles in telogen, exhibited strong CPS responses, whereas 4-, 11-, and 16-week-old mice with a predominance of anagen follicles in a large area of their integument exhibited lower responses. This suggests that the development of CPS is inhibited in mice with anagen hair follicles. Antigen-specific, T-cell receptor V beta 7+ suppressor T cells, which are recognized to down-regulate the CPS response to TCSA, were not generated in sensitized anagen mice. Culture supernatants of epidermal cells derived from mice with anagen hair follicles contained factor(s) that suppress in vivo the development of CPS. It was found that levels of mRNA for tumor necrosis factor alpha (TNF alpha) were markedly decreased in epidermal cells from early anagen to telogen mice, whereas message for IL-1 receptor antagonist (IL-1ra) was transcribed increasingly during this hair cycling. These findings suggest that altered keratinocyte production of these cytokines is involved in mediating the anagen-associated depression of CPS.
authors.affiliation: Department of Dermatology, Hamamatsu University School of Medicine, Japan. tokuray@hama-med.ac.jp
authors.forename: Y
authors.initials: Y
authors.lastname: Tokura
authors.forename: U
authors.initials: U
authors.lastname: Hofmann
authors.forename: S
authors.initials: S
authors.lastname: Müller-Röver
authors.forename: R
authors.initials: R
authors.lastname: Paus
authors.forename: H
authors.initials: H
authors.lastname: Wakita
authors.forename: H
authors.initials: H
authors.lastname: Yagi
authors.forename: N
authors.initials: N
authors.lastname: Seo
authors.forename: F
authors.initials: F
authors.lastname: Furukawa
authors.forename: M
authors.initials: M
authors.lastname: Takigawa
mesh_terms: D000367:Age Factors; D000818:Animals; D016207:Cytokines / Q000502:physiology; D003877:Dermatitis, Contact / Q000276:immunology*; D015870:Gene Expression; D018859:Hair Follicle / Q000276:immunology*; D006968:Hypersensitivity, Delayed / Q000276:immunology*; D007375:Interleukin-1 / Q000502:physiology; D016753:Interleukin-10 / Q000502:physiology; D015603:Keratinocytes / Q000276:immunology; D008198:Lymph Nodes / Q000166:cytology; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D012333:RNA, Messenger / Q000235:genetics; D012458:Salicylanilides / Q000276:immunology; D016176:T-Lymphocyte Subsets / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D014466:Ultraviolet Rays
chemical_list: D016207:Cytokines; D007375:Interleukin-1; D012333:RNA, Messenger; D012458:Salicylanilides; D014409:Tumor Necrosis Factor-alpha; D016753:Interleukin-10; C003390:3,3',4',5-tetrachlorosalicylanilide