Figure 3: Contribution of autoreactive IgE to atopic dermatitis pathophysiology
IgE AAb are held to contribute to the pathophysiology of atopic dermatitis (AD). Intracellular and intranuclear peptides originating from damaged cells of the epidermis can be picked up by antigen presenting cells (dendritic cells or Langerhans cells), processed and presented to naïve T cells with intermediate affinity to self-antigens in the lymph nodes. The presence of IL-4 results in class-switch of the B cells to the production of IgE (auto)antibodies. Humoral autoimmunity may enhance the sensitization and activation of FcεR-expressing cells, such as mast cells, basophils, eosinophils, dendritic cells, and Langerhans cells. The release of inflammatory mediators decreases the skin barrier function, promotes spongiosis and hyperkeratosis, and activates the sensory nerve endings via receptor signaling. The sensation of itch promotes scratching of the skin and further damage. Also, CD8+ memory T cells may participate in the pathological mechanisms by the production of granzyme B and perforin.
BAS: basophil, CLA: cutaneous lymphocyte-associated antigen, DC: dendritic cell, EOS: eosinophil, GM-CSF: granulocyte-macrophage colony-stimulating factor, HR: histamine receptor, IFN: interferon, ILC: innate lymphoid cell, LC: Langerhans cell, PGD2: prostaglandin D2, TGF: transforming growth factor, Th: T helper cell, TSLP: thymic stromal lymphopoietin