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IgE als Zielstruktur für therapeutische Intervention

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Allergologie

Zusammenfassung

Therapieprinzipien, die IgE, IgE-Rezeptorbindung oder IgE-Signaltransduktion als Zielstruktur nutzen, greifen am Ende der immunologischen Reaktionskaskade ein und verhindern die IgE-vermittelte Aktivierung von Effektorzellen der allergischen Entzündung. Möglichkeiten zur therapeutischen Intervention bestehen I) in der Blockade der IgE-vermittelten Aktivierung von Effektorzellen durch Reduktion des freien IgE und/oder Verhinderung der Bindung an den IgE-Rezeptor, II) Hemmung der IgE-Bildung durch gezielte Elimination von IgE-positiven B-Zellen oder III) Hemmung der IgE/FcεRI-vermittelten Signaltransduktion. Therapeutische Konzepte reichen von monoklonalen Antikörpern gegen freies, zirkulierendes IgE (z. B. Omalizumab, QGE031), löslichen FcεRI-Fusionsproteinen, Anti-IgE-DARPins (»designed ankyrin repeat proteins«) und Anti-IgE DARPin-IgG1-Fc-Fusionsproteinen, bis hin zur IgE-Plasmapherese. Während manche Ansätze schon fest im klinischen Alltag etabliert sind (z. B. Omalizumab), befinden sich viele noch in der klinischen oder präklinischen Entwicklung.

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Lamers, M., Spillner, E., Jakob, T. (2016). IgE als Zielstruktur für therapeutische Intervention. In: Biedermann, T., Heppt, W., Renz, H., Röcken, M. (eds) Allergologie. Springer, Berlin, Heidelberg. https://doi.org/10.1007/978-3-642-37203-2_58

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  • DOI: https://doi.org/10.1007/978-3-642-37203-2_58

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