TNF-α inhibitor persistence less costly in inflammatory arthritis

2021 ◽  
Vol 892 (1) ◽  
pp. 24-24
2013 ◽  
Vol 71 (Suppl 3) ◽  
pp. 555.1-555
Author(s):  
O.S. Ademowo ◽  
E. Collins ◽  
C. Rooney ◽  
A. van Kuijk ◽  
D. Gerlag ◽  
...  

2020 ◽  
Vol 22 (1) ◽  
Author(s):  
Yongyao Wu ◽  
Xiaomin He ◽  
Ning Huang ◽  
Jiayun Yu ◽  
Bin Shao

Abstract A20, also known as TNF-α-induced protein 3 (TNFAIP3), is an anti-inflammatory protein that plays an important part in both immune responses and cell death. Impaired A20 function is associated with several human inflammatory and autoimmune diseases. Although the role of A20 in mediating inflammation has been frequently discussed, its intrinsic link to arthritis awaits further explanation. Here, we review new findings that further demonstrate the molecular mechanisms through which A20 regulates inflammatory arthritis, and we discuss the regulation of A20 by many factors. We conclude by reviewing the latest A20-associated mouse models that have been applied in related research because they reflect the characteristics of arthritis, the study of which will hopefully cast new light on anti-arthritis treatments.


Inflammation ◽  
2016 ◽  
Vol 39 (5) ◽  
pp. 1624-1634 ◽  
Author(s):  
Wenhan Wang ◽  
Zhong Li ◽  
Qingjuan Meng ◽  
Pei Zhang ◽  
Pengcheng Yan ◽  
...  

2007 ◽  
Vol 179 (10) ◽  
pp. 7128-7136 ◽  
Author(s):  
Yumi Yamaguchi ◽  
Keishi Fujio ◽  
Hirofumi Shoda ◽  
Akiko Okamoto ◽  
Nelson H. Tsuno ◽  
...  

2018 ◽  
Vol 33 (3) ◽  
pp. 3317-3329 ◽  
Author(s):  
Weiwei Li ◽  
Wenhan Wang ◽  
Long Liu ◽  
Ruize Qu ◽  
Xiaomin Chen ◽  
...  

RMD Open ◽  
2019 ◽  
Vol 5 (1) ◽  
pp. e000711
Author(s):  
Juliane Schroeder ◽  
Kirsty Ross ◽  
Kathryn McIntosh ◽  
Shilan Jabber ◽  
Stuart Woods ◽  
...  

ObjectivesWe have previously shown mitogen-activated protein kinase phosphatase 2 (MKP-2) to be a key regulator of proinflammatory cytokines in macrophages. In the study presented here, we investigated the role of MKP-2 in inflammatory arthritis with a particular focus on neutrophils.MethodsTo achieve this, we subjected MKP-2 deficient and wild type mice to collagen antibody induced arthritis, an innate model of arthritis, and determined disease pathology. To further our investigation, we depleted neutrophils in a prophylactic and therapeutic fashion. Last, we used chemotaxis assays to analyse the impact of MKP-2 deletion on neutrophil migration.ResultsMKP-2-/- mice showed a significant increase in disease pathology linked to elevated levels of proarthritic cytokines and chemokines TNF-α, IL-6 and MCP-1 in comparison to wild type controls. This phenotype is prevented or abolished after administration of neutrophil depleting antibody prior or after onset of disease, respectively. While MCP-1 levels were not affected, neutrophil depletion diminished TNF-α and reduced IL-6, thus linking these cytokines to neutrophils. In vivo imaging showed that MKP-2-/- mice had an increased influx of neutrophils into affected joints, which was higher and potentially prolonged than in wild type animals. Furthermore, using chemotaxis assays we revealed that MKP-2 deficient neutrophils migrate faster towards a Leukotriene B4 gradient. This process correlated with a reduced phosphorylation of ERK in MKP-2-/- neutrophils.ConclusionsThis is the first study to show a protective role for MKP-2 in inflammatory arthritis.


2013 ◽  
Vol 72 (Suppl 1) ◽  
pp. A62.1-A62
Author(s):  
Anja Derer ◽  
Christina Böhm ◽  
Bettina Herbort ◽  
Sybille Böhm ◽  
Kirsten Neubert ◽  
...  

2008 ◽  
Vol 182 (1) ◽  
pp. 361-370 ◽  
Author(s):  
S. D. Yogesha ◽  
Shruti M. Khapli ◽  
Rupesh K. Srivastava ◽  
Latha S. Mangashetti ◽  
Satish T. Pote ◽  
...  

2021 ◽  
Vol 8 ◽  
Author(s):  
Jacopo Ciaffi ◽  
Dmitri Mitselman ◽  
Luana Mancarella ◽  
Veronica Brusi ◽  
Lucia Lisi ◽  
...  

The principle of ketogenic diet (KD) is restriction of carbohydrates to a maximum of 5–10% of the total daily caloric intake, aiming at shifting body metabolism toward ketone bodies. Different studies suggested promising results of KD to help patients to lose weight, to reduce insulin requirements in diabetes, to supplement cancer protocols, to treat neurological conditions and to optimize control of metabolic and cardiovascular diseases. However, literature about the anti-inflammatory properties of KD in rheumatic diseases is still limited. The beneficial effects of weight loss in patients with inflammatory arthritis can be explained by biomechanical and biochemical factors. Obesity is associated with macrophage activation and production of pro-inflammatory cytokines including TNF-α, IL-1b, and IL-6. The clinical effect of KD may be primarily attributed to improvement of insulin sensitivity. Insulin resistance is associated with an increase of TNF-α, IL-1α, IL-1β, IL-6, and leptin. Moreover, reduction of body's adipose tissue and weight loss account for part of the anti-inflammatory effects and for the impact of KD on cardiovascular health. In rheumatoid arthritis, fasting was shown to be effective in reducing disease symptoms, possibly through the production of β-hydroxybutyrate (BHB), the main ketone body. BHB may exert inhibitory effects also on IL-17 and intermittent fasting improved the clinical manifestations of psoriatic arthritis. In ankylosing spondylitis, current literature doesn't allow to draw conclusion about the effects of KD. Future prospective studies will be needed to elucidate the potential beneficial effects of KD on specific domains and clinical outcomes in patients with inflammatory arthritis.


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