title: Close relationship between T helper (Th)17 and Th2 response in murine allergic contact dermatitis.
abstract: BACKGROUND
  Repeated exposure to allergens induces chronic allergic lesions in the skin and a shift in the cutaneous cytokine milieu to T helper (Th)2.
  
  
  OBJECTIVE
  To assess the relationships between Th17 and Th2 response during allergic contact dermatitis (ACD) in mice.
  
  
  METHODS
  ACD was induced in C57BL/6 mice by single or repeated epicutaneous challenge of 2,4,6-trinitro-1-chlorobenzene. Relationships between Th17 and Th2 response were analyzed by immunohistochemical observations and activity of cytokines on days 8 (first challenge), 18 (11th challenge), 28 (21st challenge) and 38 (31st challenge).
  
  
  RESULTS
  On day 8, tissue levels of interleukin (IL)-17 and IL-22 were high, whereas tissue levels of IL-4 and serum IgE concentration were low. Following acute contact dermatitis, mice developed chronic eczematous lesions on day 18, and gradually improved on days 28 and 38. Tissue IL-4 and serum IgE levels corresponded to the development and improvement of chronic eczematous lesions. Numbers of Th17 cells and tissue levels of IL-17 and IL-22 rapidly decreased as IL-4 and IgE levels increased on day 18. As levels of IL-4 and IgE decreased, the number of Th17 cells and tissue levels of IL-17 and IL-22 increased again on days 28 and 38. On day 18, tissue levels of Th17 response-inducing cytokines (IL-6, IL-23 and transforming growth factor-β) were high, and IL-23-expressing cells appeared in abundance, when Th2 response was extremely high. IL-17 injection decreased tissue IL-4 and serum IgE levels.
  
  
  CONCLUSIONS
  Th17 correlates closely with Th2 in murine chronic ACD induced by repeated epicutaneous challenge.
authors.affiliation: Department of Food and Nutrition Science, Sagami Women's Junior College, Sagamihara, Japan.
authors.forename: A
authors.initials: A
authors.lastname: Matsushita
authors.forename: M
authors.initials: M
authors.lastname: Seike
authors.forename: T
authors.initials: T
authors.lastname: Hagiwara
authors.forename: A
authors.initials: A
authors.lastname: Sato
authors.forename: H
authors.initials: H
authors.lastname: Ohtsu
mesh_terms: D000208:Acute Disease; D000485:Allergens / Q000276:immunology / Q000633:toxicity; D000818:Animals; D016207:Cytokines / Q000378:metabolism*; D017449:Dermatitis, Allergic Contact / Q000276:immunology* / Q000473:pathology; D004195:Disease Models, Animal; D007073:Immunoglobulin E / Q000378:metabolism; D051379:Mice; D008810:Mice, Inbred C57BL; D010853:Picryl Chloride / Q000276:immunology / Q000633:toxicity; D058504:Th17 Cells / Q000378:metabolism*; D018418:Th2 Cells / Q000378:metabolism*
chemical_list: D000485:Allergens; D016207:Cytokines; D007073:Immunoglobulin E; D010853:Picryl Chloride