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Pathogenese des atopischen Ekzems

Pathogenesis of atopic dermatitis

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Zusammenfassung

Das atopische Ekzem (AE) zählt in Deutschland zu den häufigsten chronisch-entzündlichen Erkrankungen und ist einer der Hauptgründe, einen Hautarzt aufzusuchen. In den letzten Jahren wuchs das Kenntnis um die zellulären, molekularen und immunologischen Zusammenhänge sowie genetischen Veränderungen rasant. Dies ermöglicht ein besseres Verständnis der Erkrankung. Konsequenterweise befinden sich aktuell innovative zielgerichtete Therapien in klinischer Entwicklung bzw. bereits in der Zulassung. Um aber diese neuen Therapien sinnvoll einsetzen zu können, ist ein noch genaueres Verständnis der Pathogenese wichtig. In Zukunft werden die Stratifizierung von Patienten mit AE und die daraus folgende personalisierte Therapie an Bedeutung gewinnen. In der vorliegenden Übersicht wird der aktuelle Kenntnisstand der komplexen Pathogenese des AE dargestellt.

Abstract

Atopic dermatitis (AD) is one of the most common chronic inflammatory diseases and is also one of the most frequent reasons to consult a dermatologist. Over the past few years there has been a rapidly growing understanding of the cellular, molecular and immunological relationships as well as genetic variations, which leads to a better comprehension of the disease. Consequently, there are innovative targeted therapies in clinical studies or already approved for therapy. To make reasonable use of the new targeted therapies a good understanding of the pathogenesis is very important. In the future, stratification of patients with AD and the resulting personalized therapies will gain in importance. This review depicts the up to date state of knowledge on the complex pathogenesis of AD.

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Abbreviations

AD:

„Atopic dermatitis“

AE:

Atopisches Ekzem (Neurodermitis)

AMP:

Antimikrobielle Peptide

FLG:

Filaggrin (Strukturprotein)

HR4:

Histamin-4-Rezeptor

IDEC:

Inflammatorische dendritische epidermale Zellen

Ig:

Immunglobulin

IL:

Interleukin

LEKTI:

„Lympho-epithelial Kazal-type-related inhibitor“

S. aureus :

Staphylococcus aureus

Th-Zellen:

T-Helfer-Zellen

TSLP:

„Thymic stromal lymphopoietin“

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Correspondence to K. Eyerich.

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C. Scheerer und K. Eyerich geben an, dass kein Interessenkonflikt besteht.

Dieser Beitrag beinhaltet keine von den Autoren durchgeführten Studien an Menschen oder Tieren.

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Scheerer, C., Eyerich, K. Pathogenese des atopischen Ekzems. Hautarzt 69, 191–196 (2018). https://doi.org/10.1007/s00105-018-4127-4

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