scholarly journals Genetic predictors of response to anti-tumor necrosis factor drugs in rheumatoid arthritis

2009 ◽  
Vol 1 (1) ◽  
pp. 1
Author(s):  
Rachael Joo Lee Tan ◽  
Anne Barton
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Predictors Of Response ◽  
Genetic Predictors ◽  
Necrosis Factor

scholarly journals TREATMENT RESPONSE PREDICTION IN PATIENTS WITH RHEUMATOID ARTHRITIS. Review

2020 ◽  
Vol 16 (1) ◽  
pp. 67-76
Author(s):  
D.L. Fedkov ◽  
M.O. Komkina
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Disease Activity ◽  
Treatment Response ◽  
Adhesion Molecule ◽  
Tumor Necrosis ◽  
Response To Treatment ◽  
Predictors Of Response ◽  
Tnf Α ◽  
Necrosis Factor

Relevance. A variety of targeted therapies for rheumatoid arthritis (RA) treatment exist. Therefore, reliable predictors are needed that could be used to accurately predict the efficacy or inefficacy of these therapies in individual patients. This could allow clinicians to improve diagnosis and prognosis, to make the treatment personalized and to reduce healthcare expenses. Objectives: to analyze and systemize the predictors of response to treatment in patients with RA. Materials and Methods. We analyzed the recently discovered predictors of treatment response in RA patients using papers cited on PubMed, Lilacs, and EMBASE databases from Jan 2005 until Jan 2020.  Predictive factors were grouped into four categories: methotrexate (MTX)-treated RA, tumor necrosis factor (TNF)-α inhibitors-treated RA, interleukin (IL)-6 inhibitors-treated RA, and rituximab (RTX)-treated RA. Results. Based on the results of several studies, predictors of response to methotrexate were high Disease Activity Score (DAS), concentration of myeloid-related proteins 8/14, high P-glycoprotein levels, low serum calprotectin and leptin levels, baseline serum concentration of tumor necrosis factor (TNF)-α, TNF receptor I, interleukin (IL)-1β, soluble CD163, numbers of CD14+highCD16, vascular cell adhesion molecule, lower expression of hsa-miR-132-3p, hsa-miR-146a-5p, and hsa-miR-155-5p. A positive response to biological therapy was determined by male gender, younger age, lower health assessment questionnaire, erythrocyte sedimentation rate or C-reactive protein, neutrophil-to-lymphocyte ratio, platelet-to-lymphocyte ratio, tender joint count (or swollen joint count) scores, absence of comorbidities, baseline albumin, IL-34, IL-1β, D-dimer, fibrinogen, matrix metalloproteinase 3, DAS 28 and Simplified Disease Activity Index (SDAI). The plasma interferon (IFN) activity and the IFN beta/alpha ratio, IL-1Ra level were predictive in TNF antagonist-treated patients. Predictors of response to IL-6 inhibitors were anti–citrullinated protein antibody (ACPA)+, baseline Sharp/van der Heijde score, myeloid soluble intercellular adhesion molecule 1, serum levels of sIL-6R, IL-8, calprotectin, and lymphoid activation and bone remodeling markers. The prediction of the best response for rituximab was determined to be a combination of IL-33, rheumatoid factor or ACPA, IgG, and also lower number of previous biological therapies. Genetic factors, such as single-nucleotide polymorphisms at gene locus rs10919563, rs11541076, rs12083537, rs11265618, and rs1801274, and rs396991 can also be used to predict a response to treatment. Conclusions. One of the leading problems in the development of predictors remains the collection of high-quality and complete information from a large number of patients. For this, it is necessary to develop an digital program for collecting specific data (depending on the specific disease) and developing new algorithms for predicting the response to treatment.

The Effects of Tumor Necrosis Factor Inhibitors on Cardiovascular Risk in Rheumatoid Arthritis

2012 ◽  
Vol 18 (11) ◽  
pp. 1502-1511 ◽  
Author(s):  
Mike J.L. Peters ◽  
Alper M. van Sijl ◽  
Alexandre E. Voskuyl ◽  
Naveed Sattar ◽  
Yvo M. Smulders ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Cardiovascular Risk ◽  
Tumor Necrosis Factor ◽  
Tumor Necrosis ◽  
Tumor Necrosis Factor Inhibitors ◽  
Necrosis Factor

scholarly journals Mesenchymal stem cell-originated exosomal lncRNA HAND2-AS1 impairs rheumatoid arthritis fibroblast-like synoviocyte activation through miR-143-3p/TNFAIP3/NF-κB pathway

2021 ◽  
Vol 16 (1) ◽  
Author(s):  
Yuhua Su ◽  
Yajing Liu ◽  
Chao Ma ◽  
Chunxiao Guan ◽  
Xiufen Ma ◽  
...  
Keyword(s):  
Rheumatoid Arthritis ◽  
Tumor Necrosis Factor ◽  
Western Blot ◽  
Tumor Necrosis ◽  
Cell Counting ◽  
Biological Behavior ◽  
Luciferase Reporter ◽  
Enzyme Linked Immunosorbent Assay ◽  
Binding Interaction ◽  
Necrosis Factor

Abstract Background Long non-coding RNA heart and neural crest derivatives expressed 2-antisense RNA 1 (HAND2-AS1) was found to be elevated in rheumatoid arthritis (RA) fibroblast-like synoviocytes (RA-FLSs). However, whether HAND2-AS1 functions as an exosomal lncRNA related to mesenchymal stem cells (MSCs) in RA progression is unknown. Methods The expression of HAND2-AS1, microRNA (miR)-143-3p, and tumor necrosis factor alpha-inducible protein 3 (TNFAIP3) was detected using quantitative real-time polymerase chain reaction and Western blot. Cell proliferation, apoptosis, migration, and invasion were detected using cell counting kit-8, flow cytometry, and wound healing and transwell assays. The levels of tumor necrosis factor-α (TNF-α) and interleukins (IL)-6 were analyzed using enzyme-linked immunosorbent assay. The level of phosphorylated-p65 was examined by Western blot. The binding interaction between miR-143-3p and HAND2-AS1 or TNFAIP3 was confirmed by the dual-luciferase reporter and RIP assays. Exosomes were isolated by ultracentrifugation and qualified by transmission electron microscopy (TEM), nanoparticle tracking analysis (NTA), and Western blot. Results HAND2-AS1 was lowly expressed in RA synovial tissues, and HAND2-AS1 re-expression suppressed the proliferation, motility, and inflammation and triggered the apoptosis in RA-FLSs via the inactivation of NF-κB pathway. Mechanistically, HAND2-AS1 directly sponged miR-143-3p and positively regulated TNFAIP3 expression, the target of miR-143-3p. Moreover, the effects of HAND2-AS1 on RA-FLSs were partially attenuated by miR-143-3p upregulation or TNFAIP3 knockdown. HAND2-AS1 could be packaged into hMSC-derived exosomes and absorbed by RA-FLSs, and human MSC-derived exosomal HAND2-AS1 also repressed above malignant biological behavior of RA-FLSs. Conclusion MSC-derived exosomes participated in the intercellular transfer of HAND2-AS1 and suppressed the activation of RA-FLSs via miR-143-3p/TNFAIP3/NF-κB pathway, which provided a novel insight into the pathogenesis and treatment of RA.

Sign in / Sign up

Export Citation Format

Share Document