Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis

Hong, Yeon Sik; Moon, Su Jin; Joo, Young Bin; Jeon, Chan Hong; Cho, Mi La; Ju, Ji Hyeon; Oh, Hyeyoung; Heo, Yu Jung; Park, Sung Hwan; Kim, Ho Youn; Min, Jun Ki

doi:10.3346/jkms.2011.26.9.1132

Cited by 106 publications

(86 citation statements)

References 29 publications

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“…Therefore, data from animal models do not provide univocal evidence. In RA patients, IL-33 serum levels are increased compared to normal and disease controls (OA and psoriatic arthritis (PsA)) [21][22][23][24]. Evidence from RA SF is conflicting as IL-33 was found to be either increased [25] or comparable [23] to OA SF.…”

Section: New Members Of Il-1 Family Il-33mentioning

confidence: 98%

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

et al. 2017

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In recent years, the landscape of pro- and anti-inflammatory cytokines has rapidly expanded with the identification of new members proven to be involved at different extent in the pathogenesis of chronic immune mediated inflammatory diseases including rheumatoid arthritis (RA). The advance of our understanding of mediators involved in the pathogenesis of RA and in consequence, the development of novel targeted therapies is necessary to provide patients not responding to currently available strategies with novel compounds. The aim of this review article is to provide an overview on recently identified cytokines, emphasizing their pathogenic role and therapeutic potential in RA. A systematic literature review was performed to retrieve articles related to every cytokine discussed in the review. In some cases, evidence from animal models and RA patients is already consistent to move forward into drug development. In others, conflicting observation and the paucity of data require further investigations.Forty years after the discovery of IL-1, the landscape of cytokines is continuously expanding with increasing possibilities to develop novel therapeutic strategies in RA. Electronic supplementary material The online version of this article (10.1186/s41927-017-0001-8) contains supplementary material, which is available to authorized users.

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Section: New Members Of Il-1 Family Il-33mentioning

confidence: 98%

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

et al. 2017

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“…A previous study revealed that serum IL-33 levels were elevated in sera and synovial fluid samples from patients with rheumatoid arthritis (RA), and the levels correlated with disease activity [29][30][31][32][33][34][35][36][37]. IL-33 is produced mainly in inflamed joints [29].…”

Section: Discussionmentioning

confidence: 99%

Soluble ST2 as a marker of disease activity in systemic juvenile idiopathic arthritis

et al. 2013

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To assess the role of interleukin (IL)-33 and ST2, the receptor for IL-33, in the pathogenesis of systemic juvenile idiopathic arthritis (s-JIA), we sequentially measured the serum levels of IL-33 and soluble ST2 (sST2) in patients with s-JIA and determined their correlation with measures of disease activity and severity. Twenty-four patients with s-JIA, 5 with rheumatoid factor positive polyarticular JIA (RF + poly-JIA), and 20 age-matched healthy controls (HCs) were analyzed. IL-33 and sST2 levels were quantified in serum by enzyme-linked immunosorbent assays. Serum IL-33 levels in most patients with active s-JIA were below the lowest detection limit. Serum IL-33 levels in patients with RF + poly-JIA were significantly higher than those in patients with s-JIA and HC. Serum sST2 levels in patients during the active phase of s-JIA were much higher than those in patients with poly-JIA and HC. Serum sST2 levels in patients with s-JIA were significantly elevated even in the inactive phase, when other clinical parameters were normalized. Serum sST2 levels correlated positively with the clinical parameters of disease activity. These findings indicate that ST2 may be an important mediator in s-JIA. Serum sST2 levels in patients with s-JIA correlated with disease activity, suggesting a potential role as a promising indicator of disease activity.

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“…This result suggested that differences in the IL-33 levels of local synovial tissues from RA patients may exacerbate inflammation in RA patients. Indeed, the IL-33 levels in sera and synovial fluids are significantly higher than those in normal subjects or OA patients [1,2]. …”

Section: Discussionmentioning

confidence: 99%

“…Aside from tumor necrosis factor alpha (TNF-α) and interleukin (IL)-6, IL-33 is reportedly an important cytokine in the pathogenesis of RA. IL-33 levels in the serum and synovial fluids from RA patients are significantly higher than in samples from patients with osteoarthritis (OA) or normal subjects [1,2]. Xu et al [3 ]demonstrated that IL-33 treatment exacerbates K/BxN-induced arthritis in mice, and ST2 knockout mice developed attenuated arthritis induced by K/BxN sera.…”

Section: Introductionmentioning

confidence: 99%

Interleukin-33 Synergistically Enhances Immune Complex-Induced Tumor Necrosis Factor Alpha and Interleukin-8 Production in Cultured Human Synovium-Derived Mast Cells

Kashiwakura¹,

Yanagisawa

Lee

et al. 2013

Int Arch Allergy Immunol

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Background: Substantial evidence suggests that human synovial mast cells (MCs) are involved in the pathogenesis of rheumatoid arthritis (RA). Interleukin (IL)-33 is believed to play an important role in the pathogenesis of RA. We recently reported that FcγRI is responsible for producing abundant tumor necrosis factor alpha (TNF-α) from cultured synovium-derived MCs (SyMCs) in response to aggregated immunoglobulin G (IgG). However, whether or not IL-33 affects immune complex (IC)-induced synovial MC activation remains unknown. This study sought to evaluate the effect of IL-33 on IC-induced synovial MC activation. Methods: Cultured SyMCs were generated by culturing synovial cells with stem cell factor. ST2 expression was analyzed using FACS and immunohistochemical techniques. Mediators released from the MCs were measured using EIAs or ELISAs. Results: SyMCs obtained from patients with RA or osteoarthritis (OA) expressed ST2 on their surfaces. We confirmed the expression of ST2 in MCs using immunofluorescence staining in joint tissue obtained from RA patients. IC-triggered histamine release was not enhanced by IL-33. However, IL-33 synergistically enhanced IC-induced IL-8 and TNF-α production in SyMCs. Conclusions: ICs and IL-33 may exacerbate inflammation associated with RA by abundantly producing TNF-α and IL-8 from SyMCs.

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Measurement of Interleukin-33 (IL-33) and IL-33 Receptors (sST2 and ST2L) in Patients with Rheumatoid Arthritis

Cited by 106 publications

References 29 publications

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

Cytokines in the pathogenesis of rheumatoid arthritis: new players and therapeutic targets

Soluble ST2 as a marker of disease activity in systemic juvenile idiopathic arthritis

Interleukin-33 Synergistically Enhances Immune Complex-Induced Tumor Necrosis Factor Alpha and Interleukin-8 Production in Cultured Human Synovium-Derived Mast Cells

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