الفهرس | Only 14 pages are availabe for public view |
Abstract Summary and Conclusion Rheumatoid arthritis (RA) is a long-term inflammatory autoimmune disorder that primarily affects joints. It typically results in warm, swollen, and painful joints. Most commonly, the wrist and hands are involved, with the same joints typically involved on both sides of the body. The disease may also affect other parts of the body. This may result in a low red blood cell count, inflammation around the lungs, and inflammation around the heart. While the cause of rheumatoid arthritis is not clear, it is believed to involve a combination of genetic and environmental factors. Inflammation is a central hallmark of RA joint disease, and evidence for inflammatory pathway dysregulation and cell dysfunction has been observed in almost all innate and adaptive immune cells. Rheumatoid arthritis is considered as an autoimmune disease since the production of the rheumatoid factor (RF) which is an autoantibody directed against determinants on the Fc fragment of immunoglobulin IgG but the most relevant autoantibodies appear to be anti-citrullinated protein antibodies (ACPA). High-mobility group box protein 1 (HMGB1) was an important molecule in the pathogenesis of arthritis. Intranuclear HMGB1 binds DNA and regulates transcription. In addition, HMGB1 may be extracellularly translocated, thereby acting as an inflammatory mediator of tissue invasion and tissue repair. |