Abstract
Atopic dermatitis (AD) is a common inflammatory skin disease often associated with co-morbidities including allergic hypersensitivity. We have studied induced AD-like disease in NC/Nga mice using the hapten FITC. Following FITC-treatment the NC/Nga mice develop AD-like skin lesions in regard to the histopathological and immunological changes. Consistent with AD in humans the number of CD4+ T cells within the blood and draining lymph nodes increases considerably. To evaluate the contribution of TH cells on disease development we examined the effect of CD4 depletion. Following CD4 depletion the mice still develop AD-like skin lesions characterized by e.g. increased epidermal proliferation, hyperkeratosis and cellular infiltrate, however, the underlying immunological mechanisms change. CD4 depletion results in increased IL-17A and IL-22 production, which traditionally are associated with TH17 cells. Using confocal microscopy, we demonstrate that epidermal CD8+ cells are positive for IL-17A, indicating that these cells are TC17 cells, the cytotoxic T cell counterpart to TH17 cells. In conclusion, we show that NC/Nga mice develop AD-like disease following CD4 depletion. This is mirrored by an increased production of IL-17A, which we suggest are produced by TC17 cells. These findings support that CD8+ T cells can play a role in AD.
Published Version
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