Immune dysregulation in atopic dermatitis.

Atopic dermatitis (AD) is a chronic, relapsing, highly pruritic, inflammatory skin disease characterized by cutaneous hyperreactivity to environmentals triggers. Recent data suggest the presence of two different forms of AD: an extrinsic AD with elevated IgE involving 70-80% of the patients and an intrinsic AD with serum IgE not elevated and no specific IgE. Patients with extrinsic AD have elevated Th2- and decreased Thl-expressing cells in the peripheral blood, with elevated IL-4 and IL-13 expression, as well as IL-5. On the contrary, the intrinsic AD is linked with much lower levels of IL-4 and IL-13. Genetic factors are involved in the control of the disease and in the intrinsic AD the same chromosomal regions seem to be associated with psoriasis susceptibility. The AD is characterized by a complex of immunological alterations involving interactions between IgE-bearing antigen-presenting cells, T-cell activation, mast-cell degranulation, keratinocytes, eosinophils, and a combination of immediate and cellular immune responses. Inflammatory dendritic epidermal cells constitute a distinct dendritic cells population that is mainly found in AD and could induce the Th2/Thl isotopic switch contributing to AD chronic phase. Therapy is based on interventation in the pathophysiology of atopic eczema and elimination of exogenous provocation factors.