Rheumatoid arthritis and non-coding RNAs; how to trigger inflammation.

Area of Science:

• Immunology
• Molecular Biology
• Rheumatology

Background:

• Rheumatoid arthritis (RA) is a chronic systemic inflammatory disease characterized by joint synovitis and immune response dysregulation.
• RA pathogenesis involves complex interactions of immune cells and signaling molecules, leading to cartilage and bone damage.
• The disease process includes modifications in innate and adaptive immunity, autoantibody formation, and epitope spreading.

Purpose of the Study:

• To review current knowledge on rheumatoid arthritis pathogenesis.
• To explore the role of non-coding RNAs (ncRNAs) in RA immune responses.
• To identify potential ncRNA biomarkers for RA diagnosis and treatment.

Main Methods:

• Literature review of studies on RA pathogenesis.
• Analysis of the involvement of innate and adaptive immune cells in RA.
• Examination of the function of microRNAs (miRNAs), long non-coding RNAs (lncRNAs), and circular RNAs (circRNAs) in RA.

Main Results:

• Immune cell dysregulation, including T and B lymphocytes, macrophages, and dendritic cells, drives RA.
• Non-coding RNAs (ncRNAs) are key regulators of immune cell function and inflammatory responses.
• Emerging evidence highlights ncRNAs as potential diagnostic and therapeutic targets for RA.

Conclusions:

• Understanding RA pathogenesis is crucial for developing effective treatments.
• Non-coding RNAs represent a promising area for novel RA biomarker discovery.
• Further research into ncRNAs could lead to improved diagnostic tools and therapies for rheumatoid arthritis.