[Immunopathogenesis of systemic lupus erythematosus].

Immunpathogenese des systemischen Lupus erythematodes.
Antibodies BLyS/BAFF Immune complexes Interferon Plasma cells

Journal

Zeitschrift fur Rheumatologie
ISSN: 1435-1250
Titre abrégé: Z Rheumatol
Pays: Germany
ID NLM: 0414162

Informations de publication

Date de publication:
13 May 2022
Historique:
accepted: 13 04 2022
entrez: 13 5 2022
pubmed: 14 5 2022
medline: 14 5 2022
Statut: aheadofprint

Résumé

Insights into the immunopathogenesis of systemic lupus erythematosus (SLE) help to understand the complex disease patterns and to develop new treatment strategies. The disease manifestations essentially result from autoantibodies, immune complexes and cytokines. Particularly the propensity towards developing various autoantibodies is central to the disease itself; autoantibody specificities lead to highly variable organ manifestations. This review article delineates the clinically relevant state of knowledge on SLE pathogenesis, with the goal to establish a model useful for clinical practice, which also helps to classify the novel therapeutic approaches. Das Verständnis der Immunpathogenese des systemischen Lupus erythematodes (SLE) hilft, das komplexe Krankheitsgeschehen zu verstehen und neue Therapiestrategien zu entwickeln. Die Krankheitsmanifestationen des SLE sind im Wesentlichen Folge von Autoantikörpern, Immunkomplexen und Zytokinen. Insbesondere die Neigung zu unterschiedlichen Autoantikörpern macht das Wesen der Erkrankung aus; die genauen Spezifitäten der Autoantikörper führen zu ganz unterschiedlichen Organmanifestationen. Diese Übersichtsarbeit stellt den klinisch relevanten Stand des Wissens zur SLE-Pathogenese dar – mit dem Ziel, ein für den klinischen Einsatz nützliches Modell zu etablieren, das auch hilft, die neuen Therapieansätze einzuordnen.

Autres résumés

Type: Publisher (ger)
Das Verständnis der Immunpathogenese des systemischen Lupus erythematodes (SLE) hilft, das komplexe Krankheitsgeschehen zu verstehen und neue Therapiestrategien zu entwickeln. Die Krankheitsmanifestationen des SLE sind im Wesentlichen Folge von Autoantikörpern, Immunkomplexen und Zytokinen. Insbesondere die Neigung zu unterschiedlichen Autoantikörpern macht das Wesen der Erkrankung aus; die genauen Spezifitäten der Autoantikörper führen zu ganz unterschiedlichen Organmanifestationen. Diese Übersichtsarbeit stellt den klinisch relevanten Stand des Wissens zur SLE-Pathogenese dar – mit dem Ziel, ein für den klinischen Einsatz nützliches Modell zu etablieren, das auch hilft, die neuen Therapieansätze einzuordnen.

Identifiants

pubmed: 35551439
doi: 10.1007/s00393-022-01214-4
pii: 10.1007/s00393-022-01214-4
doi:

Types de publication

English Abstract Journal Article

Langues

ger

Sous-ensembles de citation

IM

Informations de copyright

© 2022. The Author(s).

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Auteurs

Martin Aringer (M)

Rheumatologie, Medizinische Klinik III und UniversitätsCentrum für Autoimmun- und Rheumatische Erkrankungen (UCARE), Universitätsklinikum und Medizinische Fakultät Carl Gustav Carus, TU Dresden, Fetscherstr. 74, 01307, Dresden, Deutschland. martin.aringer@uniklinikum-dresden.de.

Stephanie Finzel (S)

Klinik für Rheumatologie und Klinische Immunologie & Centrum für chronische Immundefizienz, Universitätsklinikum Freiburg, Freiburg, Deutschland.

Reinhard E Voll (RE)

Klinik für Rheumatologie und Klinische Immunologie & Centrum für chronische Immundefizienz, Universitätsklinikum Freiburg, Freiburg, Deutschland.

Classifications MeSH