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Staphylococcal exotoxins induce interleukin 22 in human th22 cells
Margarete Niebuhr1, Julia Mainardy, Annice Heratizadeh
1Department of Dermatology and Allergy, Division of Immunodermatology and Allergy Research, Hannover Medical School, Hannover, Germany.
International Archives of Allergy and Immunology
|October 11, 2014
Summary
Staphylococcal exotoxins, like SEB and α-toxin, can induce IL-22 in memory T cells and Th22 cells. This finding is crucial for understanding chronic skin inflammation in atopic dermatitis (AD).
Area of Science:
- Immunology
- Dermatology
- Microbiology
Background:
- Previous studies showed T cells from atopic dermatitis (AD) patients produce more IL-22 upon staphylococcal exotoxin stimulation.
- The specific role of staphylococcal exotoxins on polarized memory T helper (Th)22 cells in AD skin inflammation was unclear.
Purpose of the Study:
- To investigate IL-22 production in human memory T cells and polarized Th22 cells in response to staphylococcal enterotoxin B (SEB) and α-toxin.
Main Methods:
- Investigated IL-22 induction in human peripheral blood-derived CD4+CD45RO+CD45RA- T cells and polarized Th22 cells.
- Stimulated cells with SEB and sublytic α-toxin in a time-dependent manner.
- Measured IL-22 at mRNA and protein (ELISA) levels.
Main Results:
- Th22 cells secreted more IL-22 than freshly isolated memory T cells.
- SEB and α-toxin induced IL-22 in both memory T cells and Th22 cells.
- Freshly isolated memory T cells showed higher IL-22 induction by SEB and α-toxin compared to cultured Th22 cells. No differences were observed between AD, psoriasis, and healthy control cells.
Conclusions:
- Staphylococcal exotoxins can promptly induce IL-22 in skin-infiltrating memory T cells.
- This IL-22 induction may amplify chronic skin inflammation in AD, especially with bacterial colonization.
- Further investigation in lesional skin of AD and psoriasis patients is warranted.
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