TNF Inhibitor Therapy for Rheumatoid Arthritis

Ma, Xixi; Xu, Shengqian

doi:10.4172/scientificreports.155

Cited by 31 publications

(45 citation statements)

References 19 publications

(24 reference statements)

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…The effects of a TNF-α inhibitor may be dependent on TNF-α expression in synovial joints and infiltration by inflammatory cells that produce TNF-α. (66) B-cell targeted therapy includes rituximab, a chimeric monoclonal antibody that targets the CD20 surface molecule of some B cells. Its mechanism of action in RA is not completely understood.…”

Section: Discussionmentioning

confidence: 99%

A systematic review of the association of obesity with the outcomes of inflammatory rheumatic diseases

Lee¹,

Kwan²,

Lim³

et al. 2019

smedj

View full text Add to dashboard Cite

This was a systematic review of the literature on the association between obesity and the outcome of inflammatory rheumatic diseases. We conducted a literature search using PubMed®, Embase and PsycINFO®. Articles were classified into three categories based on the effects of obesity on the outcomes of inflammatory rheumatic diseases. The subject population, country, type of studies, number of patients, measurement of obesity and outcomes assessed were presented. Quality was appraised using Kmet et al's criteria. 4,331 articles were screened and 60 were relevant to the objective. Obesity had a negative, positive and neutral association with outcomes of inflammatory rheumatic diseases in 38 (63.3%) studies with 57,612 subjects, 11 (18.3%) studies with 3,866 subjects, and 11 (18.3%) studies with 3,834 subjects, respectively. In most studies, the disease population had been diagnosed with rheumatoid arthritis (RA). Tumour necrosis factor-α inhibitors were mostly associated with negative outcomes. More studies examining subjects outside Europe and North America and diseases other than RA are warranted.

show abstract

Section: Discussionmentioning

confidence: 99%

A systematic review of the association of obesity with the outcomes of inflammatory rheumatic diseases

Lee¹,

Kwan²,

Lim³

et al. 2019

smedj

View full text Add to dashboard Cite

show abstract

“…20 This hypothesis has been successfully supported by CFA-induced arthritic animal models, 21,22 and also provided the rationale for clinical trials of anti-TNF-a therapy in patients with RA. 23,24 Moreover, TNF-a is expressed in the lining of the synovial membrane at the time of arthritis onset. 20 Therefore, various strategies to modulate and inhibit TNF-a activity and expression are now being clinically applied and have been shown to be effective in the early phase of arthritic inflammation in RA.…”

Section: Discussionmentioning

confidence: 99%

The Fluence Effects of Low-Level Laser Therapy on Inflammation, Fibroblast-Like Synoviocytes, and Synovial Apoptosis in Rats with Adjuvant-Induced Arthritis

Hsieh

Cheng

Huang

et al. 2014

Photomedicine and Laser Surgery

View full text Add to dashboard Cite

Objective: The aim of this study was to evaluate the effect of low-level laser therapy (LLLT) operating at low and high fluences on joint inflammation, fibroblast-like synoviocytes (FLS), and synovial apoptosis in rats with adjuvant-induced arthritis. Background data: Rheumatoid arthritis (RA) is characterized by pronounced inflammation and FLS proliferation within affected joints. Certain data indicate that LLLT is effective in patients with inflammation caused by RA; however, the fluence effects of LLLT on synovium are unclear. Methods: Monoarthritis was induced in adult male Sprague-Dawley rats (250-300 g) via intraarticular injection of complete Freund's adjuvant (CFA) into the tibiotarsal joint. Animals were irradiated 72 h after CFA administration with a 780 nm GaAlAs laser at 4.5 J/cm 2 (30 mW, 30 sec/spot) and 72 J/cm 2 (80 mW, 180 sec/spot) daily for 10 days. After LLLT, the animals were euthanized and their arthritic ankles were collected for histopathological analysis, immunoassays of tumor necrosis factor (TNF)-a, matrix metallopeptidase (MMP)3 and 5B5, and terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assays. Results: LLLT at a fluence of 4.5 J/cm 2 significantly reduced infiltration of inflammatory cells and expressions of TNF-a-, MMP3-and 5B5-like immunoreactivities, as well as resulting in more TUNEL-positive apoptotic cells in the synovium. No significant changes were observed in these biochemicals and inflammation in arthritic animals treated with 72 J/cm 2 . Conclusions: LLLT with low fluence is highly effective in reducing inflammation to sites of injury by decreasing the numbers of FLS, inflammatory cells, and mediators in the CFA-induced arthritic model. These data will be of value in designing clinical trials of LLLT for RA.

show abstract

“…Although TNFα plays an essential role in an effective immune response, its' unrestricted production may lead to several inflammatory disorders. Inhibition of TNFα by pharmacological agents has proven to be effective in palliative treatment [10,11].…”

Section: Introductionmentioning

confidence: 99%

Development and Characterization of a Potent Tumor Necrosis Factor-Alpha Blocking Agent

Jameei

Nagarajan

Sarikhani

et al. 2019

Preprint

View full text Add to dashboard Cite

Tumor necrosis factor-α (TNFα), one of the major pro-inflammatory cytokines, plays a key role in an effective immune response. However, the chronic presence of TNFα can lead to several inflammatory disorders like rheumatoid arthritis, psoriasis, Crohn’s disease etc. Inhibition of TNFα by pharmacological inhibitors or antibodies has proven to be effective in palliative treatment to some extent. The aim of this study was to develop an anti-TNFα antibody which may be used as a therapeutic option to inhibit TNFα-mediated cytotoxicity. We characterized several hybridoma clones secreting monoclonal antibodies (mAbs) to human-TNFα. Four mAbs rescued L929 fibroblast cells from TNFα-triggered cell death and one of these, namely C8 was found to have the highest affinity. To gain insights into the mechanism by which mAb C8 inhibits human TNFα-mediated toxicity, the epitope corresponding to the mAb was delineated. The antigenic determinant was found to comprise of the stretch of amino acids 99-120, of which, 102-104 (QRE) form the core epitope. The observation was supported by bioinformatics analyses of an antigen-antibody complex model. In addition, the binding affinity of mAb C8 to TNFα was found to be comparable with that of Infliximab which is a commercially available anti TNFα mAb.

show abstract

TNF Inhibitor Therapy for Rheumatoid Arthritis

Cited by 31 publications

References 19 publications

A systematic review of the association of obesity with the outcomes of inflammatory rheumatic diseases

A systematic review of the association of obesity with the outcomes of inflammatory rheumatic diseases

The Fluence Effects of Low-Level Laser Therapy on Inflammation, Fibroblast-Like Synoviocytes, and Synovial Apoptosis in Rats with Adjuvant-Induced Arthritis

Development and Characterization of a Potent Tumor Necrosis Factor-Alpha Blocking Agent

Contact Info

Product

Resources

About