Cellular targets of interleukin-18 in rheumatoid arthritis

Dai, Sheng‐Ming; Shan, Zhengzheng; Xu, Huji; Nishioka, Kusuki

doi:10.1136/ard.2006.067793

Cited by 45 publications

(31 citation statements)

References 78 publications

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“…On the contrary, anti-IL-23 antibody treatment suppressed osteoclast differentiation, inflammation, bone destruction, and ultimately ameliorated collagen-induced arthritis (Table 1) [51]. Although IL-18 has been reported to suppress osteoclastogenesis, several studies have indicated that IL-18 is involved in bone destruction [52], wherein, IL-18 stimulates osteoclast differentiation by upregulating RANKL production from T cells in RA synovitis (Table 1). IL-18 is able to induce expression of both soluble and membrane bound RANKL [53].…”

Section: Interleukin-23 and Interleukin-18mentioning

confidence: 99%

Pro-inflammatory Cytokines Modulating Osteoclast Differentiation and Function

Seong

Kim

2016

J Rheum Dis

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In general, bone homeostasis is maintained through the balance between bone formation and resorption. Disruption in this balance results in bone-related diseases such as osteopetrosis, osteoporosis, and rheumatoid arthritis. Often, enhanced osteoclastogenesis is followed by accelerated bone resorption that is induced by pro-inflammatory cytokines in osteoporosis or rheumatoid arthritis, and leads to bone destruction. In this review study, factors involved in osteoclast differentiation and function are discussed, and how the prevention of such factors is effective in ameliorating bone loss in osteoporosis or rheumatoid arthritis.

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Section: Interleukin-23 and Interleukin-18mentioning

confidence: 99%

Pro-inflammatory Cytokines Modulating Osteoclast Differentiation and Function

Seong

Kim

2016

J Rheum Dis

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“…In the RA synovium, the expression of IL-18 is associated with that of IL-1β and TNF-α and is correlated with the acute-phase response, demonstrating that IL-18 is an important proinflammatory cytokine that drives the local production of IL-1β and TNF-α in RA patients (Joosten et al, 2003). Dai et al (2007) reported that contributes to the development and maintenance of an acquired immune response in RA by promoting the differentiation and chemotaxis of T cells. All these reports indicate that IL-18 plays an important role in the pathogenesis of RA.…”

Section: Introductionmentioning

confidence: 99%

Association of IL-18 polymorphisms with rheumatoid arthritis: a meta-analysis

Xf²,

et al. 2016

Genet. Mol. Res.

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ABSTRACT. , an important proinflammatory cytokine, has been reported to play a potential pathological role in rheumatoid arthritis (RA). Results from previous studies on the association between IL-18 polymorphisms and RA are conflicting. To clarify this, an updated meta-analysis of all available studies on IL-18 polymorphisms and RA was conducted. Eligible articles were identified by searching databases, including PubMed, Ovid, Cochrane Library, EMBASE, and China Knowledge Resource Integrated Database, for the period up to May 1, 2015. The pooled odds ratios (ORs) with 95% confidence intervals (95%CIs) were used to assess the strength of association in the homozygote, heterozygote, dominant, recessive, and additive models. The software STATA (Version 13.0) was used for statistical analysis. Finally, 14 articles were included in the present meta-analysis. The IL-18 -607C/A polymorphism showed pooled ORs and 95%CIs for the homozygote model (AA vs CC: OR = 0.598; 95%CI = 0.395-0.907), and the association between the IL-18 -137G/C polymorphism and RA showed pooled ORs and 95%CIs for the homozygote (CC vs GG: OR = 0.699; 95%CI = 0.364-1.342) and heterozygote (CG vs GG: OR = 0.924; 95%CI = 0.803-1.064) models. In summary, the current meta-analysis, which was based on the most current studies, showed that the -607A/C, -920C/T, and -105A/C polymorphisms in IL-18 were significantly associated with increased RA risk. However, the -137C/G polymorphism was not associated with RA risk under any genetic model. More evidence is needed to support or deny such a conclusion.

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“…IL-18 was reported to play an important role in RA process and therapy [9][10][11]. In RA, IL-18 is mainly produced by macrophages [12]. IL-18 activates T cells and macrophages to produce proinflammatory cytokines, chemokines, and adhesion molecules, which in turn maintain chronic inflammation and induce bone and cartilage destruction [12].…”

Section: Introductionmentioning

confidence: 99%

“…In RA, IL-18 is mainly produced by macrophages [12]. IL-18 activates T cells and macrophages to produce proinflammatory cytokines, chemokines, and adhesion molecules, which in turn maintain chronic inflammation and induce bone and cartilage destruction [12]. Vascular endothelial growth factor (VEGF) plays an important role in angiogenesis in rheumatoid synoviocytes [13].…”

Section: Introductionmentioning

confidence: 99%