CD8 T cells regulated by CD4CD25 regulatory T cells in the early stage exacerbate the development of Dermatophagoides farinae-induced skin lesions via increasing mast cell infiltration in mice.

Atopic dermatitis is a chronic inflammatory skin disease associated with CD4 Th2 cell-shifted immune responses. Although the infiltration of skin lesions by CD8 T cells has been recognized, their roles have not been fully defined. In this study, we examined the relationship between CD4 and CD8 cells in antigen-induced skin lesions of mice.

Topical skin treatment with Fab fragments of an allergen-specific IgG1 monoclonal antibody suppresses allergen-induced atopic dermatitis-like skin lesions in mice.

Fab fragments (Fabs), which lack effector functions due to the absence of the Fc portion, maintain the ability to bind to specific allergens. In the present study, we examined whether Fabs of an allergen-specific IgG1 monoclonal antibody (mAb) were able to regulate allergen-induced atopic dermatitis-like skin lesions in mice. BALB/c mice passively sensitized with ovalbumin (OVA)-specific IgE mAb were repeatedly challenged with OVA applied to the skin after sodium dodecyl sulfate treatment.

Thymic stromal lymphopoietin-induced interleukin-17A is involved in the development of IgE-mediated atopic dermatitis-like skin lesions in mice.

Atopic dermatitis (AD) is a chronic inflammatory skin disease associated with elevated levels of allergen-specific IgE. Although thymic stromal lymphopoietin (TSLP) and interleukin-17A (IL-17A) have been considered as important factors in allergic diseases, their relationships in AD have not been fully defined. Here, we show the contribution of TSLP-induced IL-17A responses to IgE-mediated AD-like skin lesions.