TABLE 12.

Immunological disturbances in AD and their resultant clinical manifestationsa

Cell typeMediatorbDirect effectbClinical manifestation
Th2IL-13IgE isotype switching↑ Serum IgE levels
↑ VCAM expressionMigration of mononuclear cells and eosinophils to lesions
IL-4IgE isotype switching↑ Serum IgE levels
Inhibits IFN-γ productionPolarizes response towards Th2
Inhibits differentiation of Th1 cells
Induces low-affinity IgE (CD23) receptor expression on macrophagesIgE binding to macrophages, via CD23, induces secretion of leukotrienes, IL-1, and TNF-α and so contributes to inflammation
IL-5Enhances differentiation, migration, and survival of eosinophilsMigration of eosinophils into lesions
Monocytes↑ IL-10, ↑ PGE2Inhibit IFN-γ productionPolarize response toward Th2
Mast cellsIL-4Drives Th to Th2Polarizes response toward Th2
Langerhans’ cellsHigh- and low-affinity (CD23) IgE receptorsBinding of allergen and presentation to T cellsContributes to inflammation in lesions
KeratinocyteIL-1, TNF-α and IL-4Induction of adhesion molecules within the skinMigration of lymphocytes, macrophages, and eosinophils into lesions, sustaining inflammation
GM-CSF and TNF-α↑ Number and antigen-presenting ability of dendritic cells in skinContributes to the chronicity of lesions
GM-CSFEnhances survival and function of monocytes, lymphocytes, and eosinophils
Eosinophils and macrophagesIL12Switch toward Th1 responseLesions become lichenified and develop epidermal hyperplasia and dermal fibrosis
  • a Data from references 249, 250, and 473

  • b PGE, prostaglandin E; GM-CSF, granulocyte-macrophage colony-stimulating factor; VCAM, vascular cell adhesion molecule.