Rheumatoid Arthritis: Molecular Mechanisms and Immunotherapy

Dear  Colleagues,

Rheumatoid arthritis (RA) is a progressive autoimmune disorder that displays genetic, pathophysiological and clinical heterogeneity. The pathogenesis of RA is primarily due to the activation of both innate and adaptive immune systems and the overproduction of a plethora of pro-inflammatory cytokines such as TNF-α, IL-1β, IL-8, IL-12, IL-17, IL-18 and IL-23. The dysregulated interaction of various cell types, cytokines and mediators leads to a constant pro-inflammatory background that promotes the propensity to break autotolerance and develop chronic synovial inflammation, bone erosion and cartilage destruction.

The advent of novel therapeutic avenues such as biological disease-modifying anti-rheumatic drugs (bDMARDs) and targeted synthetic DMARDs (tsDMARDs), including Janus kinase inhibitors, has made a breakthrough in RA treatment, but many unmet demands remain. The benefit from bDMARDs and tsDMARDs is often accompanied by severe adverse effects. In addition, personalized responsiveness to inflammatory cytokine inhibitors is observed. These facts further emphasize the need to develop novel treatment strategies for RA.

This Special Issue aims to provide a platform for the latest research clarifying the molecular and immune mechanisms underlying pathological events related to the clinical presentation and different treatment outcomes of RA. Understanding the individual variations in RA pathogenesis at the molecular level will considerably improve patient management and outcomes. Original articles and reviews revealing the inflammatory pathways, the variations in molecular mechanisms in RA pathogenesis and potential new immune-based therapy that targets specific molecular pathways involved in RA inflammation are welcome.

Prof. Dr. Irena Manolova
Guest Editor

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• rheumatoid arthritis
• pathogenesis
• innate immunity
• adaptive immunity
• inflammation
• cytokines
• autoantibodies
• immunotherapy
• clinical outcome