[Pathogenesis of atopic dermatitis].
Atopic dermatitis (AD) is a familial inflammatory skin disorder, which is characterized by extreme pruritus, the typical morphology and distribution, the chronic or chronically relapsing course, and the personal or family case history of atopy (asthma, allergic rhinitis, atopic dermatitis); moreover, we find a variety of additional features, which are either less specific or relatively rare. Although this disease has been well-known since the beginning of the century, we have not clearly understood its pathogenesis so far. This article reviews the reported deviations of the immune system and the alterations of the mediators of inflammation as well as the abnormalities of cyclic nucleotide regulation. These findings are correlated to the clinical symptoms. The following topics have been dealt with in detail: association with HLA-antigens, elevation of serum IgE and generation of IgE immune complexes, numerical and functional deficiencies of T-suppressor cells, involvement of granulocytes, alterations of mediators of inflammation, and particularly, observations on the cAMP-phosphodiesterase. These extremely complex findings, which are based on the interaction between disregulation of the autonomous nervous system and alterations of the immune system, may provide a better understanding of the pathogenesis of atopic dermatitis.
D000242:Cyclic AMP / Q000378:metabolism; D003876:Dermatitis, Atopic / Q000235:genetics / Q000276:immunology*; D006636:Histamine Release; D006801:Humans; D007111:Immunity, Cellular; D007073:Immunoglobulin E / Q000032:analysis; D009504:Neutrophils / Q000276:immunology; D012306:Risk
D007073:Immunoglobulin E; D000242:Cyclic AMP
Zur Pathogenese der Atopischen Dermatitis.