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Role of genetic alterations in the NLRP3 and CARD8 genes in health and disease
Örebro universitet, Institutionen för hälsovetenskap och medicin.ORCID-id: 0000-0002-4589-6440
Örebro universitet, Institutionen för hälsovetenskap och medicin.ORCID-id: 0000-0002-0278-4510
Örebro universitet, Institutionen för hälsovetenskap och medicin.ORCID-id: 0000-0002-9826-0462
2015 (engelsk)Inngår i: Mediators of Inflammation, ISSN 0962-9351, E-ISSN 1466-1861, artikkel-id 846782Artikkel i tidsskrift (Fagfellevurdert) Published
Abstract [en]

The complexity of a common inflammatory disease is influenced by multiple genetic and environmental factors contributing to the susceptibility of disease. Studies have reported that these exogenous and endogenous components may perturb the balance of innate immune response by activating the NLRP3 inflammasome. The multimeric NLRP3 complex results in the caspase-1 activation and the release of potent inflammatory cytokines, like IL-1β. Several studies have been performed on the association of the genetic alterations in genes encoding NLRP3 and CARD8 with the complex diseases with inflammatory background, like inflammatory bowel disease, cardiovascular diseases, rheumatoid arthritis, and type 1 diabetes. The aim of the present review is therefore to summarize the literature regarding genetic alterations in these genes and their association with health and disease.

sted, utgiver, år, opplag, sider
New York: Hindawi Publishing Corporation, 2015. artikkel-id 846782
Emneord [en]
NLRP3, inflammasome, polymorphism, CARD8
HSV kategori
Forskningsprogram
Biomedicin
Identifikatorer
URN: urn:nbn:se:oru:diva-42795DOI: 10.1155/2015/846782ISI: 000350655400001Scopus ID: 2-s2.0-84924227184OAI: oai:DiVA.org:oru-42795DiVA, id: diva2:789480
Merknad

Funding Agencies:

Magnus Bergvalls Foundation

Sigurd and Elsa Goljes Minne (Lindhes Advokatbyrå AB)

Stiftelsen Gamla Tjänarinnor

Tilgjengelig fra: 2015-02-19 Laget: 2015-02-19 Sist oppdatert: 2018-01-11bibliografisk kontrollert

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Paramel, GeenaSirsjö, AllanFransén, Karin

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