Efficacy and safety of monoclonal antibodies targeting interleukin-17 pathway for inflammatory arthritis: a meta-analysis of randomized controlled clinical trials

Wei, Min; Duan, Dongmei

doi:10.2147/dddt.s91374

Cited by 22 publications

(17 citation statements)

References 54 publications

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“…However, adverse events of the treatment should be realized, such as impaired peripheral immune tolerance, reduction in natural killer (NK) cells, increased pulmonary embolism and hemorrhagic stroke . In addition, interleukin‐17 (IL‐17) has been demonstrated to play important roles in RA, and targeting IL‐17 gives potential therapy . It is notable that treatment on RA patients with monoclonal antibodies against IL‐17 may cause adverse effects, including diarrhea, leukemia, laryngeal abscess, interstitial lung disease and brachial plexopathy .…”

Section: Introductionmentioning

confidence: 99%

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

et al. 2019

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Aim This study aims to discuss plasma and messenger RNA (mRNA) levels of interleukin (IL)‐37 in rheumatoid arthritis (RA) patients and evaluate the potential of plasma IL‐37 as a biomarker for RA. Method Plasma IL‐37 levels and IL‐37 mRNA relative concentrations were measured by enzyme‐linked immunosorbent assay (ELISA) and quantitative reverse transcriptase‐polymerase chain reaction (RT‐PCR). We discussed the association of IL‐37 levels and clinical, laboratory parameters in RA patients in a training cohort. Plasma IL‐37 levels were tested for discriminatory capacity by receiver operating characteristic (ROC) curve analysis. We then validated plasma IL‐37 expression in a cohort of 598 patients (230 RA, 107 systemic lupus erythematosus [SLE], 100 osteoarthritis [OA], 62 gout, 51 primary Sjögren's syndrome [pSS], 48 ankylosing spondylitis [AS]). Results Both plasma levels of IL‐37 and mRNA levels of IL‐37 were elevated in RA patients compared to those in healthy controls in the training cohort, and there was a good diagnostic ability to predict RA (area under the curve [AUC] = 0.97). Plasma IL‐37 levels were significantly related to Disease Activity Score of 28 joints ‐ erythrocyte sedimentation rate (DAS28‐ESR) (rs = 0.459, P < 0.001). The levels of IL‐37 mRNA were related to plasma IL‐37 levels (rs = 0.642, P < 0.001), DAS28‐ESR (r = 0.641, P < 0.001) and C‐reactive protein (rs = 0.603, P < 0.001). In the validation cohort, when plasma IL‐37 in RA patients compared with that in SLE, OA, gout, pSS and AS patients, the AUC was 0.86, 0.87, 0.91, 0.87, 0.92, respectively. Conclusion IL‐37 expression was increased in RA patients, and correlated with disease activity. IL‐37 may be a biomarker for the diagnosis of RA.

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Section: Introductionmentioning

confidence: 99%

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

et al. 2019

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“…Lee et al [16] reported that the number of Th17 cells in RA patients was significantly higher than that in the control group, and the amount of synovial fluid was related to the serum IL-17A level and the severity of joint damage. Blocking IL-17A and TNF-α has a synergistic effect on inhibiting IL-6 production and collagen degradation in RA synovial fluid and synovial fluid [17]. Therefore, Th17 cells can be used as a new target for the treatment of RA.…”

Section: Th17 Cells and Rheumatoid Arthritismentioning

confidence: 99%

Research Progress of Th17/Treg Cells and Their Transcription Factors in Autoimmune Diseases

Hou¹,

Mu²,

Wang³

2019

AJCEM

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Helper T cell 17 (Th17) being a new cell subset of CD4+T in the body, which is different from Th1 and Th2 cells, have independent mechanisms of differentiation and developmental regulation. Th17 cells mainly secrete various cytokines such as IL-17, IL-6 and TNF-α, which induce inflammation. Treg cells are T cells with high expression of CD25 differentiated by T cells under the action of certain cytokines, namely CD4+CD25+(hi) Foxp3+T cells, which can regulate the immune response mediated by effector cells and are an important line of defense for human autoimmune. Therefore, Treg cells play an important role in maintaining immune tolerance of the body. As an important subset of T cells, Treg cells have an inhibitory effect on inflammation. Its working principle is to selectively inhibit autoreactive T cells and effector T cells so as to maintain the body's immune balance, and normal quantity and function help the immune system to its antigen stimulation, establishing a good state of tolerance. The expression of Treg cells increased, can avoid the occurrence of autoimmune diseases. Treg cells inhibit the differentiation of Th17 cells by down-regulating the expression of IL-23 and IL-17 or by its specific transcription factor Foxp3; similarly, inhibition of Th17 cell production can promote the development of Treg cells. Both Th17 and Treg cells are functionally inhibited. Th17 cells promote inflammatory reaction, and Treg cells suppress immune reaction. Numerous cytokines are involved in regulation. For example, IL-6 and IL-21 can inhibit Foxp3 and promote the expression of RORγt, thereby inhibiting Treg cells and inducing the differentiation of Th17 cells. In the absence of IL-6 and other pro-inflammatory factors, TGF-β enhances the inhibitory effect of Foxp3 on RORγt and promotes the growth and development of Treg cells. The anti-inflammatory factor IL-10 also induces Treg cells to inhibit the reaction of Th17 cells. The effects of Treg and Th17 cells are normally in a dynamic equilibrium. Once the balance is imbalanced, autoimmune diseases will occur. This article reviews the differentiation, function and research progress of Th17/Treg cells in autoimmune diseases.

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“…Specifically, IL-17-blocking antibody significantly reduced ACR20 and ACR50. It also dramatically reduced DAS28, an index that measures tenderness and swelling severity of joints [Wei and Duan, 2016].…”

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confidence: 99%

Altered Expression of MicroRNAs in Rheumatoid Arthritis

Tavasolian

Abdollahi

Rezaei

et al. 2017

J of Cellular Biochemistry

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Rheumatoid arthritis is one of the most common types of inflammatory joint diseases. Women, smokers, and people with positive family history are more susceptible to this disease. Diagnostic criteria include at least one swollen joint that has not been caused by other diseases. MicroRNAs are non-coding RNAs that are evolutionarily conserved and have a length of 18-25 nucleotides. MicroRNAs control gene expression at the post-transcriptional level via promoting mRNA degradation or translational repression. Recognition of alterations in microRNA status and their respective targets, may offer an opportunity to better identify the pathways that are involved in the etiopathogenesis of autoimmune diseases. It has been suggested that microRNAs may serve as potential biomarkers for both diagnosis and prognosis of autoimmune diseases. Here, we review the available evidence on the deregulations of microRNA expression in rheumatoid arthritis. More precisely, this review focuses on the microRNA involved in T cell regulation and gives perspectives on the use of this microRNA as biomarkers of diagnosis, prognosis, or intervention efficacy. J. Cell. Biochem. 119: 478-487, 2018. © 2017 Wiley Periodicals, Inc.

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Efficacy and safety of monoclonal antibodies targeting interleukin-17 pathway for inflammatory arthritis: a meta-analysis of randomized controlled clinical trials

Cited by 22 publications

References 54 publications

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

Elevated expression of interleukin‐37 in patients with rheumatoid arthritis

Research Progress of Th17/Treg Cells and Their Transcription Factors in Autoimmune Diseases

Altered Expression of MicroRNAs in Rheumatoid Arthritis

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