Abstract
Since 1966 when K. Ishizaka and co-workers [42] first detected cytophilic immunoglobulin E (IgE) as the carrier of reaginic activity in the sera of allergic patients, the production of IgE against common and otherwise innocuous antigens has been recognized as a central feature in the pathogenesis of immediate type hypersensitivity. In order to understand the reasons for this pathological immune response, the regulation of IgE production has become the subject of intensive investigation. Confined as they were to in vitro systems, studies of human IgE synthesis proved to be rather problematic. Until lately, they were restricted to spontaneous IgE secretion by plasma cells which had differentiated in vivo. As opposed to IgG, measurement of the extremely small amounts of IgE secreted into culture supernatants was impeded by the limited specificity and sensitivity of the detection methods. In addition, results were often influenced by cytophilic IgE released from cells bearing Fc receptors for IgE (FcεR), such as B lymphocytes, monocytes and basophils. Only the development of monoclonal antibody techniques and the rapid progress in molecular biology have facilitated a deeper understanding of the mechanisms of IgE regulation. Since this insight was obtained in humans as well as in rodent models, in the following chapter the results from the human and the animal systems will be summarized separately from each other. Nevertheless, this juxtaposition will demonstrate that despite some species-specific differences, many of the findings in rodents apply to human IgE synthesis also.
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Prinz, J.C., Rieber, E.P. (1991). Regulation of IgE Synthesis. In: Ruzicka, T., Ring, J., Przybilla, B. (eds) Handbook of Atopic Eczema. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-662-02671-7_16
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