Journal Article DZNE-2020-04076

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The inflammasomes and autoinflammatory syndromes.

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2015
Annual Reviews Palo Alto, Calif.

Annual review of pathology 10(1), 395-424 () [10.1146/annurev-pathol-012414-040431]

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Abstract: Inflammation, a vital response of the immune system to infection and damage to tissues, can be initiated by various germline-encoded innate immune-signaling receptors. Among these, the inflammasomes are critical for activation of the potent proinflammatory interleukin-1 cytokine family. Additionally, inflammasomes can trigger and maintain inflammatory responses aimed toward excess nutrients and the numerous danger signals that appear in a variety of chronic inflammatory diseases. We discuss our understanding of how inflammasomes assemble to trigger caspase-1 activation and subsequent cytokine release, describe how genetic mutations in inflammasome-related genes lead to autoinflammatory syndromes, and review the contribution of inflammasome activation to various pathologies arising from metabolic dysfunction. Insights into the mechanisms that govern inflammasome activation will help in the development of novel therapeutic strategies, not only for managing genetic diseases associated with overactive inflammasomes, but also for treating common metabolic diseases for which effective therapies are currently lacking.

Keyword(s): Animals (MeSH) ; Autoimmune Diseases: immunology (MeSH) ; Humans (MeSH) ; Inflammasomes: immunology (MeSH) ; Inflammation: immunology (MeSH) ; Syndrome (MeSH) ; Inflammasomes

Classification:

Contributing Institute(s):
  1. Innate Immunity in Neurodegeneration (AG Latz)
Research Program(s):
  1. 342 - Disease Mechanisms and Model Systems (POF3-342) (POF3-342)

Appears in the scientific report 2015
Database coverage:
Medline ; Allianz-Lizenz / DFG ; BIOSIS Previews ; BIOSIS Reviews Reports And Meetings ; Clarivate Analytics Master Journal List ; IF >= 15 ; JCR ; NCBI Molecular Biology Database ; NationallizenzNationallizenz ; SCOPUS ; Science Citation Index Expanded ; Web of Science Core Collection
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Document types > Articles > Journal Article
Institute Collections > BN DZNE > BN DZNE-AG Latz
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 Record created 2020-02-18, last modified 2024-03-21



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