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

TLDR
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

Serum levels of IL-33 and its receptor ST2 are elevated in patients with ankylosing spondylitis.

TL;DR: Serum levels of IL-33 could partially reflect AS disease activity and indicate that IL- 33/ST2 signalling plays an important role in the pathogenesis of AS.
Journal ArticleDOI

miR-487b mitigates chronic heart failure through inhibition of the IL-33/ST2 signaling pathway

TL;DR: Estimation of the effects of microRNA-587b in a rat model of chronic heart failure found that it reduces apoptosis, inflammatory responses, and fibrosis in CHF by suppressing IL-33 through inhibition the IL- 33/ST2 signaling pathway.
Journal ArticleDOI

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

TL;DR: Interleukin (IL)-33 synergistically enhanced IC-induced IL-8 and TNF-α production in SyMCs, and ICs and IL-33 may exacerbate inflammation associated with RA by abundantly producing T NF-α andIL-8 fromSyMCs.
Journal Article

Serum levels of soluble ST2 and interleukin-33 in patients with dermatomyositis and polymyositis.

TL;DR: Sera sST2 levels were significantly higher in DM and PM patients and correlated with CRP, CK, LDH and VAS, and data support that s ST2 may play a role inDM and PM.
References
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Journal Article

Revised criteria for the classification of rheumatoid arthritis.

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.
Journal ArticleDOI

IL-33, an interleukin-1-like cytokine that signals via the IL-1 receptor-related protein ST2 and induces T helper type 2-associated cytokines

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.
Journal ArticleDOI

Role of proinflammatory cytokines in the pathophysiology of osteoarthritis

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.
Journal ArticleDOI

Disease-associated functions of IL-33: the new kid in the IL-1 family.

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.
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