Abstract
Atopic dermatitis (AD) is a chronic inflammatory skin disease frequently associated with bronchial asthma and/or allergic rhinitis in the patient or a member of the immediate family. The etiopathogenesis of the inflammatory skin lesions is largely unknown. Clinical observations and recent research results,however,point to a dysfunction in the cellular immunoregulation [11]. AD patients are more susceptible to bacterial, viral, and mycotic skin infections. From a clinical point of view, this indicates a localized defect in the immune system. Patients with certain primary immune defects (such as Wiskott-Aldrich syndrome, ataxia teleangiectasia, hyper-IgF syndrome, or X-chromosomal hypogammaglobulinemia) may show eczematous skin lesions that cannot be distinguished from those of AD. These diseases and AD have further been observed to show a characteristic rise in the level of serum IgE. In addition to increased IgE synthesis, multiple abnormalities, including decreased number of circulating CD8+ T cells and CD16+ natural killer (NK) cells, impaired autologous mixed lymphocyte reactions, and depressed granulocyte and monocyte chemotaxis, have been described in AD patients. AD is characterized by strongly elevated IgE levels compared to other atopic diseases, and a proportion of this IgE is specific for antigens, which may act as exacerbating factors in the disease. Antigen-induced exacerbations may be mediated by either antigen presentation by Langerhans cells to T cells or cutaneous mast cell mediator release. This assumption is further supported by the finding that patients with AD may show eczematous patch-test reactions to aeroallergens.
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Reinhold, U. (1997). Atopic Dermatitis. In: Burg, G., Dummer, R.G. (eds) Strategies for Immunointerventions in Dermatology. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-60752-3_21
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DOI: https://doi.org/10.1007/978-3-642-60752-3_21
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