Abstract
Rheumatoid arthritis (RA) is an autoimmune disease characterized by destructive synovitis. It is significantly associated with disability, impaired quality of life, and premature mortality. Recently, the development of biological agents (including tumor necrosis factor-α and interleukin-6 receptor inhibitors) and Janus kinase inhibitors have advanced the treatment of RA; however, it is still difficult to predict which drug will be effective for each patient. To break away from the current therapeutic approaches that could be described as a “lottery,” there is an urgent need to establish biomarkers that stratify patients in terms of expected therapeutic responsiveness. This review deals with recent progress from multi-faceted analyses of the synovial tissue in RA, which is now bringing new insights into diverse features at both the cellular and molecular levels and their potential links with particular clinical phenotypes.
Highlights
Drug Selection for Patients withRheumatoid arthritis (RA) is an autoimmune disease that can impair physical function by causing persistent synovial inflammation, leading to joint destruction
In patients who previously had an inadequate response to conventional synthetic disease-modifying antirheumatic drugs (DMARDs), typically methotrexate, the outcome measures (American College of Rheumatology 20% response rate (ACR20), ACR50, and ACR70) of biological DMARDs (bDMARDs) or tsDMARDs have only been reported in about 60%, 40%, and about 20% of patients, respectively [2]
Raterman et al reported that the high expression of type I IFN network genes in the peripheral blood at baseline was associated with treatment resistance to rituximab [27], whereas Wampler et al found that higher IFN signaling in neutrophils correlates with a good response to tumor necrosis factor (TNF)-α inhibitors [28]
Summary
Rheumatoid arthritis (RA) is an autoimmune disease that can impair physical function by causing persistent synovial inflammation, leading to joint destruction. The field of RA therapy has developed disease-modifying antirheumatic drugs (DMARDs) that can be divided into biological DMARDs (bDMARDs) and targeted synthetic DMARDs (tsDMARDs) [1]. The former class includes TNF-α inhibitors, the T-cell costimulation inhibitor (CTLA4Ig; abatacept), the IL-6 receptor inhibitors, and the antibody targeted against CD20 (rituximab). This inefficient approach takes time, and during this time, there can be irreversible joint destruction. The search for biomarkers that predict the treatment responsiveness of individual patients is an urgent task, and success here should accelerate the generation of RA therapy by optimizing the allocation of therapeutics. The Search for Therapeutic Response Predictors Using Information Obtained from
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