Danger-signaler og inflammasomer ved autoinflammatoriske og autoimmune sygdomme

Klaus Bendtzen

Danger-signaler og inflammasomer ved autoinflammatoriske og autoimmune sygdomme

Klaus Bendtzen

3 Citationer (Scopus)

Abstract

Cytoplasmic inflammasomes are formed through activation of pattern recognition receptors (PRR) of the innate immune system. Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ß-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes. These inflammasomes govern the induction of proinflammatory cytokines such as IL-1ß, IL-18 and IL-33. PRR and inflammasome dysfunctions may underly immunoinflammatory diseases such as gout and other arthritides, type 1 diabetes and arteriosclerosis.

Bidragets oversatte titel	Danger signals and inflammasomes in autoinflammatory and autoimmune diseases
Originalsprog	Dansk
Tidsskrift	Ugeskrift for Laeger
Vol/bind	173
Udgave nummer	38
Sider (fra-til)	2340-3
Antal sider	4
ISSN	0041-5782
Status	Udgivet - 2011

Emneord

Arteriosclerosis
Arthritis
Autoimmune Diseases
Cytokines
Diabetes Mellitus, Type 1
Hereditary Autoinflammatory Diseases
Humans
Immunity, Innate
Inflammasomes
Inflammation
Nod Signaling Adaptor Proteins
Receptors, Pattern Recognition
Receptors, Tumor Necrosis Factor
Toll-Like Receptors

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Link to publication in Scopus

Citationsformater

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title = "Danger-signaler og inflammasomer ved autoinflammatoriske og autoimmune sygdomme",

abstract = "Cytoplasmic inflammasomes are formed through activation of pattern recognition receptors (PRR) of the innate immune system. Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, {\ss}-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes. These inflammasomes govern the induction of proinflammatory cytokines such as IL-1{\ss}, IL-18 and IL-33. PRR and inflammasome dysfunctions may underly immunoinflammatory diseases such as gout and other arthritides, type 1 diabetes and arteriosclerosis.",

keywords = "Arteriosclerosis, Arthritis, Autoimmune Diseases, Cytokines, Diabetes Mellitus, Type 1, Hereditary Autoinflammatory Diseases, Humans, Immunity, Innate, Inflammasomes, Inflammation, Nod Signaling Adaptor Proteins, Receptors, Pattern Recognition, Receptors, Tumor Necrosis Factor, Toll-Like Receptors",

author = "Klaus Bendtzen",

year = "2011",

language = "Dansk",

volume = "173",

pages = "2340--3",

journal = "Ugeskrift for Laeger",

issn = "0041-5782",

publisher = "Almindelige Danske Laegeforening",

number = "38",

}

TY - JOUR

T1 - Danger-signaler og inflammasomer ved autoinflammatoriske og autoimmune sygdomme

AU - Bendtzen, Klaus

PY - 2011

Y1 - 2011

N2 - Cytoplasmic inflammasomes are formed through activation of pattern recognition receptors (PRR) of the innate immune system. Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ß-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes. These inflammasomes govern the induction of proinflammatory cytokines such as IL-1ß, IL-18 and IL-33. PRR and inflammasome dysfunctions may underly immunoinflammatory diseases such as gout and other arthritides, type 1 diabetes and arteriosclerosis.

AB - Cytoplasmic inflammasomes are formed through activation of pattern recognition receptors (PRR) of the innate immune system. Endogenous and exogenous danger signals, e.g. DNA- and RNA-fragments, urate- and cholesterol crystals, silica and asbestos, ß-amyloid, UV-light and skin irritants, may induce NOD-like receptor protein (NLRP)3 inflammasomes. These inflammasomes govern the induction of proinflammatory cytokines such as IL-1ß, IL-18 and IL-33. PRR and inflammasome dysfunctions may underly immunoinflammatory diseases such as gout and other arthritides, type 1 diabetes and arteriosclerosis.

KW - Arteriosclerosis

KW - Arthritis

KW - Autoimmune Diseases

KW - Cytokines

KW - Diabetes Mellitus, Type 1

KW - Hereditary Autoinflammatory Diseases

KW - Humans

KW - Immunity, Innate

KW - Inflammasomes

KW - Inflammation

KW - Nod Signaling Adaptor Proteins

KW - Receptors, Pattern Recognition

KW - Receptors, Tumor Necrosis Factor

KW - Toll-Like Receptors

UR - https://www.scopus.com/pages/publications/80355145115

M3 - Tidsskriftartikel

C2 - 21936977

SN - 0041-5782

VL - 173

SP - 2340

EP - 2343

JO - Ugeskrift for Laeger

JF - Ugeskrift for Laeger

IS - 38

ER -

Danger-signaler og inflammasomer ved autoinflammatoriske og autoimmune sygdomme

Abstract

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