Rheumatoid arthritis (RA) is a chronic autoimmune systemic inflammatory disorder that predominantly affects synovial joints, both small and large, often in a symmetric pattern. This disorder, while not directly causing death, can significantly reduce the quality of life and life expectancy of patients if left untreated.
The immunopathogenesis of rheumatoid arthritis spans multiple decades and commences with the production of autoantibodies against post-translationally modified proteins, identified as Checkpoint 1. These autoantibodies play a crucial role in the pathogenesis of the disease.
Rheumatoid arthritis is more than just a joint disorder; it can affect various body systems, including the skin, eyes, lungs, heart, and blood vessels. This extensive impact underlines the importance of understanding how the immune system functions in the context of RA. The immune system is divided into two branches: the humoral branch, which deals with extracellular fluid invasions, and the cellular branch, which deals with invasions occurring within cells.
Nature Immunology provides insights into the pathogenic role of immune cells in rheumatoid arthritis and its implications. Similarly, research published in PMC and National Center for Biotechnology Information further elaborates on the immunology of rheumatoid arthritis.
Rheumatoid arthritis affects approximately 1% of the general population and is characterized by persistent articular inflammation and joint damage. This damage is driven by proliferating synovial tissue fibroblasts, as well as neutrophil, monocyte, and lymphocyte trafficking into the synovium, as detailed in a study from PubMed.
For more comprehensive information, one can also refer to the Mayo Clinic for symptoms and causes of rheumatoid arthritis, and to RheumatoidArthritis.net for an understanding of the role of the immune system in rheumatoid arthritis.
