title: Staphylococcal-derived superantigen enhances peanut induced Th2 responses in the skin.
abstract: BACKGROUND
  The allergen-induced activation and expansion of IL-4 producing T helper type 2 (Th2) cells is a key event in the initiation and progression of allergic disease. Intriguingly, concomitant early childhood staphylococcal skin infections are being increasingly implicated in the allergen-induced switch of primary T cell responses towards the Th2 phenotype.
  
  
  OBJECTIVE
  We sought to identify whether or not staphylococcal-derived superantigen can influence the primary T cell response in the skin to food allergens with a view to determining whether such exposures create the immune pathology that predisposes to the development of food allergy.
  
  
  METHODS
  Using a novel Th2 reporter model, we determined the ability of the staphylococcal superantigen (SEB) to influence priming in the skin of IL-4 expressing Th2 cells by peanut extract (PE). Factors including the effect of SEB on the magnitude of the Th2 response in the skin draining lymph nodes, T cell receptor V region usage and the influence of endotoxin were evaluated.
  
  
  RESULTS
  Primary exposure to PE and SEB lead to significantly enhanced PE specific Th2 responses when the mice were subsequently exposed to PE alone. The enhancement of the Th2 response was dependent on the Vβ-binding properties of the SEB, but was not affected by endotoxin-mediated TLR-4 effects or strain differences in the mice.
  
  
  CONCLUSIONS
  These results identify that in the skin environment, the presence of SEB can significantly increase the numbers of allergen-induced Th2 cells which develop in response to subsequent allergen exposure. These data highlight the process by which individuals may become pathologically sensitized to food allergens in early life.
authors.affiliation: Malaghan Institute of Medical Research, Wellington South, New Zealand. eforbes-blom@malaghan.org.nz
authors.forename: E
authors.initials: E
authors.lastname: Forbes-Blom
authors.forename: M
authors.initials: M
authors.lastname: Camberis
authors.forename: M
authors.initials: M
authors.lastname: Prout
authors.forename: S-C
authors.initials: SC
authors.lastname: Tang
authors.forename: G
authors.initials: G
authors.lastname: Le Gros
mesh_terms: D000485:Allergens / Q000009:adverse effects* / Q000276:immunology / Q000494:pharmacology; D000818:Animals; D004768:Enterotoxins / Q000009:adverse effects* / Q000819:agonists / Q000276:immunology / Q000494:pharmacology; D015847:Interleukin-4 / Q000235:genetics / Q000276:immunology; D051379:Mice; D008807:Mice, Inbred BALB C; D018345:Mice, Knockout; D021183:Peanut Hypersensitivity / Q000235:genetics / Q000276:immunology* / Q000473:pathology; D011948:Receptors, Antigen, T-Cell / Q000235:genetics / Q000276:immunology; D012867:Skin / Q000276:immunology* / Q000473:pathology; D013211:Staphylococcus aureus / Q000276:immunology*; D018089:Superantigens / Q000009:adverse effects* / Q000276:immunology / Q000494:pharmacology; D018418:Th2 Cells / Q000276:immunology* / Q000473:pathology
chemical_list: D000485:Allergens; D004768:Enterotoxins; D011948:Receptors, Antigen, T-Cell; D018089:Superantigens; D015847:Interleukin-4; C031818:enterotoxin B, staphylococcal