[Pathophysiology of autoinflammatory dermatoses].

Feldmeyer, Laurence; Navarini, A A (2020). [Pathophysiology of autoinflammatory dermatoses]. Hautarzt, 71(5), pp. 333-341. Springer-Medizin-Verlag 10.1007/s00105-020-04585-4

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Autoinflammation leads to inflammation that mostly occurs without any clinically obvious reason. It can be so severe that organ damage with relevant tissue damage occurs. Inflammasomes are the drivers of autoinflammation. Although IL‑1 beta and the inflammasomes as its critical regulators are very important in autoinflammation, not all patients respond to inhibition of this signalling pathway. Several autoinflammatory diseases were associated with mutations in proteasome-immunoproteasome components. Autoinflammatory diseases caused by highly relevant genetic variants are mostly hereditary. Usually in childhood but not always. The coming years will show whether inflammatory dermatoses will be increasingly treated with suppression of the innate immune system in addition to inhibition of adaptive immunity.

Item Type:

Journal Article (Further Contribution)

Division/Institute:

04 Faculty of Medicine > Department of Dermatology, Urology, Rheumatology, Nephrology, Osteoporosis (DURN) > Clinic of Dermatology

UniBE Contributor:

Feldmeyer, Laurence

Subjects:

600 Technology > 610 Medicine & health

ISSN:

0017-8470

Publisher:

Springer-Medizin-Verlag

Language:

German

Submitter:

Sandra Nyffenegger

Date Deposited:

05 Jan 2021 08:59

Last Modified:

05 Jan 2021 08:59

Publisher DOI:

10.1007/s00105-020-04585-4

PubMed ID:

32333042

Uncontrolled Keywords:

Autoinflammation Inflammasome Interleukin Monogenic autoinflammatory diseases Proteasome

BORIS DOI:

10.48350/149484

URI:

https://boris.unibe.ch/id/eprint/149484

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