Immune dysregulation in atopic dermatitis

Atopic dermatitis (AD) is a chronic, relapsing, highly pruritic, inflammatory skin disease characterized by cutaneous liyperreactivity to environmentals triggers. Recent data suggest the presence of tivo duferent forms of AD: an extrinsic AD with elevated IgE involving 70-80% ofthe patients and an intrinsic AD with serum IgE not elevated and no specfc IgE. Patients with extrinsic AD have elevated Th2- and decreased Th1-expressing cells in the peripheral blood, with elevated IL-4 and IL-13 expression, as well as lL—5. On the contrary, the intrinsic AD is linked with much lower levels ofll.-4 and lL—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, eosino-pliils, and a combination of immediate and cellular immune responses Inflammatory dendritic epidermal cells constitute a distinct dendritic cells population that is mainlyfound in AD and could induce the Th2/Th1 isotopic switch contributing to AD chronic phase. Therapy is based on interventation in the pathophysiology of atopic eczema and elimination of exogenous provocation factors.