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