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Journal ArticleDOI

Measurement of interleukin-33 (IL-33) and IL-33 receptors (sST2 and ST2L) in patients with rheumatoid arthritis.

01 Sep 2011-Journal of Korean Medical Science (Korean Academy of Medical Sciences)-Vol. 26, Iss: 9, pp 1132-1139
TL;DR: IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA, and the levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naïve RA.
Abstract: The interleukin-33 (IL-33)/ST2 pathway has emerged as an intercellular signaling system that participates in antigen-allergen response, autoimmunity and fibrosis. It has been suggested that IL-33/ST2 signaling has been involved in the pathogenesis of rheumatoid arthritis (RA), because IL-33 and its receptor have been specifically mapped to RA synovium. The aim of this study was to determine the levels of IL-33 and sST2 in sera and synovial fluids in patients with RA. The serum level of IL-33 was significantly higher in patients with RA (294.9 ± 464.0 pg/mL) than in healthy controls (96.0 ± 236.9 pg/mL, P = 0.002). The synovial fluid level of IL-33 was significantly higher in RA patients than in osteoarthritis patients. The level of serum sST2 was higher in RA patients than in healthy controls (P = 0.042). A significant relationship was found between the levels of IL-33 and IL-1β (r = 0.311, P = 0.005), and IL-33 and IL-6 (r = 0.264, P = 0.017) in 81 RA patients. The levels of IL-33, sST2 and C-reactive protein decreased after conventional disease-modifying antirheumatic drugs treatment in 10 patients with treatment-naive RA. Conclusively, IL-33 is involved in the pathogenesis of RA and may reflect the degree of inflammation in patients with RA.

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Journal ArticleDOI
TL;DR: The aim of the present study was to examine the changes of IL‐33 and sST2 serum levels in patients with stroke.
Abstract: Aim Interleukin 33 (IL-33) functions as an alarmin and is produced by damaged tissue. It is reported that the levels of both IL-33 and its receptor, soluble suppression of tumorigenicity 2 (sST2), are elevated in some inflammatory diseases. As acute ischemic stroke causes local inflammation and a systemic immune response, the aim of the present study was to examine the changes of IL-33 and sST2 serum levels in patients with stroke. Methods Enzyme-linked immunosorbent assay was used to detect serum levels of IL-33 and sST2 in 56 healthy subjects and total 28 stroke patients on day 1, day 7, and week 3 after stroke. The correlation of changes of IL-33 and sST2 serum levels with clinical features of stroke patients was determined. Results The levels of sST2 were significantly reduced on day 1, week 1 and week 3 after stroke (P < 0.0001 at all three time-points). The levels of sST2 at week 1 and 3 were significantly correlated with 6-month modified Barthel index scores. Conclusions The serum level of sST2 could predict the recovery of stroke. IL-33 serum level might be protective from brain tissue damage of stroke. Regulation of IL-33/sST2 pathway after stroke might be related to the peripheral immune response induced by ischemic stroke.

2 citations

Journal ArticleDOI
TL;DR: In this paper, the association between IL33/ST2 gene polymorphisms and BD was investigated in 585 BD uveitis (BDU) patients and 834 healthy controls using Agena MassARRAY iPLEX platform.
Abstract: Interleukin (IL)33, a member of the IL1 superfamily, functions as a nuclear factor and mediates biological effects by interacting with the ST2 receptor. Recent studies have described IL33 as an emerging pro-inflammatory cytokine in the immune system, and IL33/ST2 gene polymorphisms have been implicated in the pathogenesis of various immune diseases. However, the underlying mechanisms of IL33/ST2 in Behcet's disease (BD) remain to be defined. Here, we investigated the association between IL33/ST2 gene polymorphisms and BD in 585 BD uveitis (BDU) patients and 834 healthy controls using Agena MassARRAY iPLEX platform. We found that rs3821204 was associated with the development of BDU. Moreover, the frequency of rs2210463 G allele was lower in patients with genital involvement. Association analysis revealed a much greater genetic difference between complete-type and incomplete-type BD groups, including three SNPs (rs7044343, rs1048274, and rs2210463). Our findings suggest that IL33/ST2 gene polymorphisms are involved in the pathogenesis of BDU. Different genetic backgrounds may exist in complete-type and incomplete-type BD patients.

2 citations

Journal ArticleDOI
12 Jul 2020
TL;DR: This review is aimed at analyzing the available information on the pathogenesis of infective endocarditis, the role of IL-33 and ST2 in the formation of the inflammatory response in various pathological processes, and changes in the expression of the genes encoding these proteins under the influence of various factors.
Abstract: An inflammatory process accompanied by a considerable number of pathological conditions in the body is one of the symptoms of infective endocarditis. The components of the immune system involved in the inflammatory response may serve as markers determining the development and prognosis of the disease and as potential therapeutic targets. These components include cytokines IL-33, sST2, and the IL-33/ST2 system, which are actively involved in the modulation of the inflammatory response. At present, the role of these biologically active molecules is well described for various pathologies associated with tissue destruction, including cardiovascular diseases, but not for the pathogenesis of infective endocarditis. This review is aimed at analyzing the available information on the pathogenesis of infective endocarditis, the role of IL-33 and ST2 in the formation of the inflammatory response in various pathological processes, and changes in the expression of the genes encoding these proteins under the influence of various factors.

1 citations

Journal ArticleDOI
01 Oct 2018
TL;DR: IL-33 is a novel potential marker for the risk of RA as well as a marker of disease activity, positively correlated with disease duration, ESR, CRP and disease severity.
Abstract: Background: Rheumatoid Arthritis (RA) is a chronic progressive, systemic inflammatory, connective tissue disease affecting approximately 1% of the general population. Interleukin-33 (IL33), a member of the IL-1 family, is a ligand for the orphan receptor ST2 (known as IL-1RL1 also). IL-33 is crucial for Th2 cytokine-mediated immune responses however; it can overcome this role in RA. Aim: This study aimed to investigate the potential role of inflammatory cytokine (IL-33) in RA and assess the correlation of IL-33 level to disease activity. Subjects and Method: The study included sixty patients with RA. Patients were diagnosed according to the American College of Rheumatology (ACR) 2010 revised criteria and were classified into 2 groups of 30 patients each according to disease activity score 28 (DAS28), the first group included RA patients with DAS28 of ≤2.4 and the second group included RA patients with DAS28 >2.4.Thirty normal subjects served as a control group. Serum IL-33 was measured using ELISA. Results: Serum IL33 level was significantly higher in patient's group compared to the control group (P ≤.001). Also, serum IL33 level, was significantly higher in patients’ group 2 (DAS>2.4) than patients’ group 1 (DAS≤2.4) (P<0.001). Serum IL-33 level positively correlated with disease duration, ESR, CRP and disease severity. Conclusion: IL-33 is a novel potential marker for the risk of RA as well as a marker of disease activity

1 citations


Cites result from "Measurement of interleukin-33 (IL-3..."

  • ...All these results confirmed the fact that IL-33/ST2 signaling played a vital role in joint inflammation of human RA and experimental CIA model(21)....

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References
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Journal ArticleDOI
TL;DR: The revised criteria for the classification of rheumatoid arthritis (RA) were formulated from a computerized analysis of 262 contemporary, consecutively studied patients with RA and 262 control subjects with rheumatic diseases other than RA (non-RA).
Abstract: The revised criteria for the classification of rheumatoid arthritis (RA) were formulated from a computerized analysis of 262 contemporary, consecutively studied patients with RA and 262 control subjects with rheumatic diseases other than RA (non-RA). The new criteria are as follows: 1) morning stiffness in and around joints lasting at least 1 hour before maximal improvement; 2) soft tissue swelling (arthritis) of 3 or more joint areas observed by a physician; 3) swelling (arthritis) of the proximal interphalangeal, metacarpophalangeal, or wrist joints; 4) symmetric swelling (arthritis); 5) rheumatoid nodules; 6) the presence of rheumatoid factor; and 7) radiographic erosions and/or periarticular osteopenia in hand and/or wrist joints. Criteria 1 through 4 must have been present for at least 6 weeks. Rheumatoid arthritis is defined by the presence of 4 or more criteria, and no further qualifications (classic, definite, or probable) or list of exclusions are required. In addition, a "classification tree" schema is presented which performs equally as well as the traditional (4 of 7) format. The new criteria demonstrated 91-94% sensitivity and 89% specificity for RA when compared with non-RA rheumatic disease control subjects.

19,409 citations


"Measurement of interleukin-33 (IL-3..." refers methods in this paper

  • ...RA was diagnosed based on the American College of Rheumatology 1987 criteria (13)....

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Journal Article
TL;DR: The Bulletin on the Rheumatic Diseases has published all of the classification criteria for the rheumatic diseases to date, and these new revised classified criteria for rheumatoid arthritis are very important as they should provide understanding of the possibly changing face of rheumatism.
Abstract: The Bulletin on the Rheumatic Diseases has published all of the classification criteria for the rheumatic diseases to date. These new revised classification criteria for rheumatoid arthritis are very important as they should provide understanding of the possibly changing face of rheumatoid arthritis.

8,645 citations

Journal ArticleDOI
01 Nov 2005-Immunity
TL;DR: A member of theIL-1 family, IL-33, which mediates its biological effects via IL-1 receptor ST 2, activates NF-kappaB and MAP kinases, and drives production of T(H)2-associated cytokines from in vitro polarized T( H)2 cells is reported.

3,306 citations


"Measurement of interleukin-33 (IL-3..." refers background in this paper

  • ...It also increases the production of IL-5 and IL-13 by polarized Th2 cells (3) and interferon-γ (IFN-γ) production by both iNKT and NK cells (7)....

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  • ...Mature IL-33 has been reported to mediate its biologic effects via T1/ST2 binding by activating NF-κB and MAP kinase (3)....

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  • ...The expression of ST2L, a membrane-anchored long form, is restricted to the surface of Th2 cells and mast cells (3)....

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  • ...Although recombinant pro-IL-33 is cleaved by recombinant caspase-1 in vitro (3), the in vivo role of caspase-1 in the cleavage of pro-IL-33 remains controversial (27)....

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  • ...Therefore, synovial fibroblasts, endothelial cells, activated DCs, and macrophages may be the main source of IL-33 in synovial fluid from RA patients (3, 15)....

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Journal ArticleDOI
TL;DR: The current knowledge regarding the role of proinflammatory cytokines in the pathophysiology of OA is discussed and the potential of anticytokine therapy in the treatment of this disease is addressed.
Abstract: Osteoarthritis (OA) is associated with cartilage destruction, subchondral bone remodeling and inflammation of the synovial membrane, although the etiology and pathogenesis underlying this debilitating disease are poorly understood. Secreted inflammatory molecules, such as proinflammatory cytokines, are among the critical mediators of the disturbed processes implicated in OA pathophysiology. Interleukin (IL)-1β and tumor necrosis factor (TNF), in particular, control the degeneration of articular cartilage matrix, which makes them prime targets for therapeutic strategies. Animal studies provide support for this approach, although only a few clinical studies have investigated the efficacy of blocking these proinflammatory cytokines in the treatment of OA. Apart from IL-1β and TNF, several other cytokines including IL-6, IL-15, IL-17, IL-18, IL-21, leukemia inhibitory factor and IL-8 (a chemokine) have also been shown to be implicated in OA and could possibly be targeted therapeutically. This Review discusses the current knowledge regarding the role of proinflammatory cytokines in the pathophysiology of OA and addresses the potential of anticytokine therapy in the treatment of this disease.

1,962 citations


"Measurement of interleukin-33 (IL-3..." refers background in this paper

  • ...IL-1β, TNF and IL-6 seem to be the main proinflammatory cytokines involved in the pathophysiology of OA (19)....

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Journal ArticleDOI
TL;DR: IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting TH2-type immune responses but can also promote the pathogenesis of asthma by expanding TH2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation.
Abstract: Interleukin-33 (IL-33), a newly described member of the IL-1 family, is expressed by many cell types following pro-inflammatory stimulation and is thought to be released on cell lysis. The IL-33 receptor, consisting of ST2 and IL-1 receptor accessory protein, is also widely expressed, particularly by T helper 2 (T(H)2) cells and mast cells. IL-33 is host-protective against helminth infection and reduces atherosclerosis by promoting T(H)2-type immune responses. However, IL-33 can also promote the pathogenesis of asthma by expanding T(H)2 cells and mediate joint inflammation, atopic dermatitis and anaphylaxis by mast cell activation. Thus IL-33 could be a new target for therapeutic intervention across a range of diseases.

925 citations


"Measurement of interleukin-33 (IL-3..." refers background in this paper

  • ...(24) also proposed that in established RA, IL-33 causes mast cell-mediated inflammation, which amplifies the Th17 cell response....

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  • ...(24) suggested that in early RA, IL-33 produced by synovial fibroblasts and synovial endothelial cells induces a Th2-type response....

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