Altered susceptibility to collagen-induced arthritis in transgenic mice with aberrant expression of interleukin-1 receptor antagonist

Ma, Yuhe; Thornton, Sherry; Boivin, Gregory P.; Hirsh, David; Hirsch, Raphael; Hirsch, Emmet

doi:10.1002/1529-0131(199810)41:10<1798::aid-art11>3.0.co;2-l

Cited by 65 publications

(21 citation statements)

References 31 publications

(25 reference statements)

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“…Granulocyte-macrophage colony stimulating factor (GM-CSF) is yet another key cytokine involved in the induction of CIA as demonstrated by GM-CSF -/-knock-out mice that were resistant to CIA while the GM-CSF+/+ littermates developed CIA [52]. Mice overexpressing IL-1Ra have a significant reduction in the incidence and severity of CIA [53]. After CII immunization, IL-1Ra mRNA is overexpressed in the spleens, but not in the joints, of transgenic mice [53].…”

Section: Collagen-induced Arthritismentioning

confidence: 99%

“…Mice overexpressing IL-1Ra have a significant reduction in the incidence and severity of CIA [53]. After CII immunization, IL-1Ra mRNA is overexpressed in the spleens, but not in the joints, of transgenic mice [53]. Minimal differences were observed in the humoral or cellular immune responses to CII.…”

Section: Collagen-induced Arthritismentioning

confidence: 99%

“…Mice lacking IL-1Ra have a significantly earlier onset of CIA, with increased severity. Thus, endogenous expression of IL-1Ra in the joint is a critical determinant of susceptibility to CIA [53]. Sera from IFN-␥ R (-/-) mice, which exhibit decreased incidence and severity of CIA, have lower levels of CII-specific IgG levels, indicatin that IFN-␥ exacerbates CIA by affecting the levels of CII-specific IgG Ab as well as by the imbalance of Th1/Th2 cells [54].…”

Section: Collagen-induced Arthritismentioning

confidence: 99%

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Animal models of rheumatoid arthritis and related inflammation

et al. 1999

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The major, extensively studied, experimentally-induced rat and mouse models of arthritis with features resembling rheumatoid arthritis are reviewed here. Etiopathogenetic studies that were recently published are emphasized. In summary, multiple triggering stimuli can induce disease in genetically-prone strains of inbred rats and mice. Multiple genetic loci, including both MHC and non-MHC, regulate disease expression in these animals. By comparison with other models of autoimmune disease, clustering of regulatory loci within and among species is increasingly becoming evident. At the cellular level, both innate and acquired immune systems are involved in the disease manifestations. At the molecular level, unbalanced chronic production of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, IL-6 and IL-12, as opposed to IL-4 and IL-10, is correlated with arthritis disease susceptibility and severity.

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Section: Collagen-induced Arthritismentioning

confidence: 99%

Section: Collagen-induced Arthritismentioning

confidence: 99%

Section: Collagen-induced Arthritismentioning

confidence: 99%

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Animal models of rheumatoid arthritis and related inflammation

et al. 1999

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“…Mice lacking IL1Ra (IL-1Ra À/À) are highly susceptible to lipopolysaccharide-induced lethality [6]. In the collagen-induced arthritis model, these mice exhibit early arthritis onset and more severe joint destruction [7]. Moreover, IL-1Ra À/À mice develop various type of spontaneous inflammatory diseases according to their genetic background [8,9].…”

Section: Introductionmentioning

confidence: 99%

Interleukin-1 plays a major role in vascular inflammation and atherosclerosis in male apolipoprotein E-knockout mice

Merhi-Soussi

Kwak

Magne

et al. 2005

Cardiovascular Research

192

122

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“…Die k. o. Mäuse zeigten außerdem eine 10fach erhöhte Expression von IL-1 mRNA im Gelenk (15). Im Gegensatz dazu zeigen Mäuse mit einer Über-expression von IL-1Ra eine verminderte Inzidenz und Schweregrad der Kollagen-induzierten Arthritis (16). Wird IL-1a oder IL-1b bei Kaninchen lokal ins Gelenk injiziert, so kann bereits nach wenigen Stunden eine Akkumulation von Leukozyten und ein Verlust von Proteoglykanen aus dem Gelenkknorpel beobachtet werden (17), welcher durch IL-1Ra inhibiert werden kann (18).…”

Section: Interleukin-1 (Il-1) Und Der Interleukin-1-rezeptorantagonisunclassified

Der Interleukin-1-Rezeptorantagonist Anakinra (Kineret�) in der Behandlung mit rheumatoider Arthritis

Rubbert-Roth

Perniok

2003

Zeitschrift f�r Rheumatologie

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New treatment strategies in rheumatoid arthritis are targeted to interfere with critical mediators of inflammation. Proinflammatory cytokines like IL-1 beta and TNFalpha play a crucial role in induction and maintenance of synovitis, pannus formation and bone and cartilage destruction. Within a few years, these morphological changes may lead to joint destruction and consecutively to functional impairment. Since April 2002 a recombinant human interleukin-1 receptor antagonist (Anakinra) is available in Germany for treatment of patients with rheumatoid arthritis. Anakinra (Kineret(R)) is approved for therapy in combination with methotrexate and should be applied according to guidelines established by the German Rheumatology Society for the use of biologicals in treatment of patients with rheumatoid arthritis. The approval of anakinra as a new therapeutic is based on data obtained in large multicenter, placebo-controlled, and randomised trials in comparison to placebo. Treatment of Anakinra as monotherapy or in combination with methotrexate lead to significant improvement of signs and symptoms of disease as measured by the ACR 20 (or more) response and was associated with a slower radiographic progression with regard to joint space narrowing and development of erosions. Anakinra showed a favourable safety profile with injection side reactions as the predominant side effect that occurs in 70% of patients usually after 10-12 days of treatment and that are mostly mild to moderate and self-limiting. Patients with previous pneumonia or other risk factors for pulmonary infections such as chronic obstructive lung disease seem to show a slightly increased risk of developing infectious complications of the bronchopulmonary system while being on anakinra and should be monitored appropriately. Combining IL-1ra treatment with the use of anti-TNF agents showed an increased risk of infectious complications in clinical studies and is not recommended at present. Studies are currently assessing the use of anakinra for treatment of other rheumatic diseases like psoriatic arthritis, juvenile arthritis or spondylarthropathy.

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Altered susceptibility to collagen-induced arthritis in transgenic mice with aberrant expression of interleukin-1 receptor antagonist

Cited by 65 publications

References 31 publications

Animal models of rheumatoid arthritis and related inflammation

Animal models of rheumatoid arthritis and related inflammation

Interleukin-1 plays a major role in vascular inflammation and atherosclerosis in male apolipoprotein E-knockout mice

Der Interleukin-1-Rezeptorantagonist Anakinra (Kineret�) in der Behandlung mit rheumatoider Arthritis

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