title: Epicutaneous sensitization with a protein antigen induces Th17 cells.
abstract: BACKGROUND
  Th17 is a newly identified effector T cell lineage which plays a central role in many human inflammatory diseases and experimental animal models. Epicutaneous sensitization with a protein antigen has been proven to induce a Th2-predominant immune response and lead to development of atopic diseases in a murine protein-patch model.
  
  
  OBJECTIVE
  We sought to assess the generation of Th17 cells in epicutaneous sensitization with a protein antigen and its regulation by environmental elements and genetic background.
  
  
  METHODS
  BALB/c, C57BL/6, and DO11.10 mice were epicutaneously immunized by patch application of the following: ovalbumin alone, or co-administration of one of TLR ligands, irritant, hapten or superantigens. IL-17 and IL-22 contents in supernatants of in vitro reactivation culture of lymph nodes cells were determined by ELISA. Frequency of IL-17-secreting CD4 T cells was measured by ELISPOT.
  
  
  RESULTS
  Small but significant amounts of IL-17 and IL-22 could be detected in supernatants of in vitro reactivation culture of lymph nodes cells of mice receiving patch application of ovalbumin. ELISPOT assay for IL-17 also revealed low frequency of IL-17-secreting CD4 T cells in lymph nodes cells in ovalbumin group. All TLR ligands tested including agonists for TLR2, TLR3, TLR4, TLR5, TLR7 and TLR9 as well as many environmental elements including irritant, hapten and superantigen could further promote the generation of Th17 cells. In addition, C57BL/6 mice generate less Th17 cells than BALB/c mice in epicutaneous sensitization.
  
  
  CONCLUSIONS
  This study demonstrates Th17 generation and its regulation by environmental elements and genetic background to a protein antigen by epicutaneous route.
authors.affiliation: Department of Dermatology, National Taiwan University Hospital and National Taiwan University College of Medicine, Taipei, Taiwan.
authors.forename: Li-Fang
authors.initials: LF
authors.lastname: Wang
authors.forename: Hsien-Ching
authors.initials: HC
authors.lastname: Chiu
authors.forename: Chih-Jung
authors.initials: CJ
authors.lastname: Hsu
authors.forename: Ching-Yi
authors.initials: CY
authors.lastname: Liu
authors.forename: Yu-Han
authors.initials: YH
authors.lastname: Hsueh
authors.forename: Shi-Chuen
authors.initials: SC
authors.lastname: Miaw
mesh_terms: D000818:Animals; D000941:Antigens / Q000276:immunology*; D015496:CD4-Positive T-Lymphocytes / Q000276:immunology; D016207:Cytokines / Q000276:immunology; D005260:Female; D006969:Hypersensitivity, Immediate / Q000235:genetics / Q000276:immunology*; D020381:Interleukin-17 / Q000235:genetics / Q000276:immunology*; D007378:Interleukins / Q000276:immunology; D008024:Ligands; D051379:Mice; D008807:Mice, Inbred BALB C; D008810:Mice, Inbred C57BL; D010047:Ovalbumin / Q000276:immunology; D012867:Skin / Q000276:immunology*; D006377:T-Lymphocytes, Helper-Inducer / Q000276:immunology* / Q000378:metabolism; D051193:Toll-Like Receptors / Q000276:immunology / Q000378:metabolism; D000097043:Interleukin-22
chemical_list: D000941:Antigens; D016207:Cytokines; D020381:Interleukin-17; D007378:Interleukins; D008024:Ligands; D010047:Ovalbumin; D051193:Toll-Like Receptors; D000097043:Interleukin-22