Chlamydia‐infected Macrophages mediate Interleukin‐23 and Tumor Necrosis Factor‐driven Reactive Arthritis in SKG Mice

2021 ◽  
Author(s):  
Xavier Romand ◽  
Xiao Liu ◽  
M Arifur Rahman ◽  
Zaied Ahmed Bhuyan ◽  
Claire Douillard ◽  
...  
2020 ◽  
Author(s):  
Asgar Barkhordaria ◽  
Karim Mahnam ◽  
Hamid Mir Mohammad Sadeghi

Abstract Background: Rheumatoid arthritis disease is a chronic autoimmune inflammatory disease that mainly causes synovial joint inflammation and cartilage destruction. Tumor necrosis factor-α (TNF-α) is a pivotal cytokine that plays an important role in rheumatoid arthritis. The treatments focusing on a single cytokine' inhibition, are able to clinically produce meaningful responses in only about half of the treated patients due to multiple cytokines involved in this disease. In the present study, a bi-specific tandem single-chain variable fragment was designed in order to suppress both human tumor necrosis factor-α and interleukin-23 (IL23) as a potential therapeutic drug candidate for this disease. To do so, at first, eight bi-specific tandem single-chain variable fragment models were built against tumor necrosis factor-α and interleukin-23 cytokines with different domain orders and then 50 ns molecular dynamics simulation was performed for each one and thereafter structural properties were exploited. Results: MD simulation results indicate that the domains' order strongly affects tandem single-chain variable fragment properties and in overall, the fragment VLIL23+Linker+VHIL23+linker+VLTNF+Linker+VHTNF +His6 (VL is variable light and VH is variable heavy fragments and His6 is six histidine) not only separated antibody domains but also had better stability and solvation energy. Conclusions: Hence, this structure can be considered as a potential drug for rheumatoid arthritis. It is hoped that this research could shed a light for the treatment of Rheumatoid arthritis disease.


2007 ◽  
Vol 29 (2-3) ◽  
pp. 187-194 ◽  
Author(s):  
Zhanju Liu ◽  
Jinxia Jiu ◽  
Shuman Liu ◽  
Xianen Fa ◽  
Fuguang Li ◽  
...  

2011 ◽  
Vol 63 (5) ◽  
pp. 1274-1280 ◽  
Author(s):  
Alain Meyer ◽  
Emmanuel Chatelus ◽  
Daniel Wendling ◽  
Jean-Marie Berthelot ◽  
Emmanuelle Dernis ◽  
...  

2020 ◽  
Vol 47 (10) ◽  
pp. 1575-1581 ◽  
Author(s):  
Bjarni Thorsteinsson ◽  
Arni J. Geirsson ◽  
Niels S. Krogh ◽  
Bjorn Gudbjornsson

Objective.Reactive arthritis (ReA) is a spondyloarthritis triggered by a bacterial infection. In cases where nonsteroidal antiinflammatory drugs and conventional synthetic disease-modifying antirheumatic drugs have failed, biologics such as tumor necrosis factor inhibitors (TNFi) have been used. However, limited evidence exists of the efficacy and safety of these drugs in ReA. We report on Icelandic patients with ReA who have been treated with TNFi, their characteristics, outcomes, and safety.Methods.We conducted an observational cohort study using the Icelandic nationwide database of biologic therapy (ICEBIO) supplemented with a retrospective study of electronic health record (EHR) data. Drug efficacy was assessed using disease activity scores and standardized questionnaires within ICEBIO; safety was assessed using ICEBIO and EHR data.Results.Thirty-eight patients with ReA were registered in the database. Eight were given TNFi within 1 year of symptom onset. At 6 and 18 months, there was a significant reduction in C-reactive protein (CRP), tender and swollen joints, visual analog scale for pain and fatigue, 28-joint count Disease Activity Score 28 based on CRP, Clinical Disease Activity Index, and Health Assessment Questionnaire scores. Seventy-one to 90% of patients were considered treatment responders. Two patients were able to stop biologics owing to remission. During the 303 patient-years (mean 8, range 1–15) biologics were given, 6 hospital admissions for infections were noted.Conclusion.TNFi are safe and effective in ReA, but treatment tends to be prolonged. Further clinical trials are urgently needed in ReA.


Sign in / Sign up

Export Citation Format

Share Document