Fig. 3.

Hypothetic cellular pathways and targets of autoreactivity in atopic dermatitis. Skin damage can lead to release of self-peptides resulting in allergic sensitization to autoantigens via antigen presentation by dendritic cells (DC) to naïve T cells and class switch of B cells. Mast cells sensitized with IgE autoantibodies can directly interfere with the self-peptides that are released following skin damage resulting in histamine release. T cells with low binding affinity to self-peptides may escape selection and depletion in the thymus. Possibly, this population of cells may also be attracted to the skin where they are exposed to the self-peptides of the damaged skin. Cytokines (IL-4 and IFN-γ) produced by T-cells, and histamine by MC can directly exacerbate the skin lesion. Additionally, neurons in the skin can bind histamine and IL-31 specifically to the histamine 1 receptor (H1R) and IL-31 receptor (IL-31R) which results in itch and may lead to the chronicity of the impaired barrier function. Th2 T helper lymphocyte, EO eosinophils, ILC2 innate lymphoid cell, IgE immunoglobulin E, IL interleukin, IFN-γ Interferon gamma, TSLP thymic stromal lymphopoietin