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ePaper created 2014-09-15, 12:31:02 | version 1.32.01
References 1. Vloten WA van, Willemze R, Lange Vejlsgaard G, et al. Cutaneous Lymphomas. Karger Publ. Basel 1990. 2. Lambert WC, Giannotti B. van Vloten WA. Basic mechanisms of physiological and abberant lymohoproliferation in the skin. Plenum Press New York, 1994. 3. Willemze R, Kerl H, Sterry W, et al. EORTC classification for primary cutaneous lymphomas: a proposal from the Cutaneous Lymphoma Study Group of the European Organization for Research and Treatment of Cancer. Blood 1997; 90: 354-71. 4. Grange F, Bekkenk MW, Wechsler J, et al. Prognostic factors inprinmary cutaneous large B-cell lymphoma: a European multicenter study. J Clinical Oncology 2001; 19: 3602-10. Allergens, atopens and reagins Allergens are a complex mixture of proteins and carbohydrates. At the department, a common structure present in many allergens - the lysine-sugar structure - was identified and denoted as the atopen.[1] For allergens containing a lot of protein, such as pollen allergens, this appeared to be less valid. However, regarding house dust allergen, this theory seemed to be quite sound. An in-vitro test was developed, based on the complement binding assay resulting in the lysis of erythrocytes, which could be used to test the potency of the allergenic extract before testing it on humans. The stronger the complement activation, the stronger the skin reactivity of the allergenic extract.[2,3] Once allergens have passed the epithelial barrier they will encounter reagins to elicit an allergic response. In the concept of Berrens, allergens are not single entities, they form a complex mixture of antigens and atopens. This evokes the theoretical question whether reagins interact with the antigen or with the atopen structure of the allergen. Regular exposure to allergens would elicit an antigen- antibody response and in addition an atopen-reagin response. In this concept, the antibody was IgE and the reagin remained a structure to be elucidated. All attempts to identify a component of an acute phase system as the responsible factor have failed. Arguments for this theory were that the interaction between an atopen and a reagin would be much faster than one between an antigen and an antibody. Moreover, UV light would be capable of destroying the atopen reagin interaction by deactivating the lysine-sugar residues (Maillard reaction), whereas the antigen-antibody interaction would not be influenced, supporting the view that allergen-free environments found at high altitude are beneficial. It was however demonstrated that UV also deactivated the binding of antigen to IgE. In the 1980s it became evident that Der p1 was the most important allergen in house dust and that it was generated by the house dust mite. The IgE antibodies that were specifically directed towards epitopes in Der p1 were called reagins. Being lysine sugar residues, the atopens have since been neglected by researchers, although they are still present in the allergen. However, a revival of the atopen concept may occur, since recently attention has been paid to the role of common sugar structures (mannose) in allergens of plants, insects and parasites. They are considered to increase the allergic response by interfering with mannose receptors on innate immune cells like dendritic cells.[4] 71 BWEADVSMGFINCORR:Opmaak 1 21-07-2014 17:40 Pagina 71