Abstract
Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic, inflammatory disorder that affects synovial joints, both small and large joints, in a symmetric pattern. This disorder usually does not directly cause death but significantly reduces the quality of life and life expectancy of patients if left untreated. There is no cure for RA but, patients are usually on long-term disease modifying anti-rheumatic drugs (DMARDs) to suppress the joint inflammation, to minimize joint damage, to preserve joint function, and to keep the disease in remission. RA is strongly associated with various immune cells and each of the cell type contributes differently to the disease pathogenesis. Several types of immunomodulatory molecules mainly cytokines secreted from immune cells mediate pathogenesis of RA, hence complicating the disease treatment and management. There are various treatments for RA depending on the severity of the disease and more importantly, the patient’s response towards the given drugs. Early diagnosis of RA and treatment with (DMARDs) are known to significantly improve the treatment outcome of patients. Sensitive biomarkers are crucial in early detection of disease as well as to monitor the disease activity and progress. This review aims to discuss the pathogenic role of various immune cells and immunological molecules in RA. This review also highlights the importance of understanding the immune cells in treating RA and in exploring novel biomarkers.
Highlights
Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic disorder that manifests as inflammation of synovial joints, leading to joint destruction and deformity
There is an increased risk of tuberculosis infection associated with use of biological disease modifying anti-rheumatic drugs (DMARDs) such as anti-tumor necrosis factor (TNF) therapy [4,5]
During activation of T-cells, CD4+ T-cells interact with human leukocyte antigen (HLA) or major histocompatibility class II (MHC-II) molecules as well as co-stimulating molecules such as CD28 that are expressed on the surface of antigen presenting cell (APC) [25]
Summary
Rheumatoid arthritis (RA) is a chronic, autoimmune, systemic disorder that manifests as inflammation of synovial joints, leading to joint destruction and deformity. There is an increased risk of tuberculosis infection associated with use of biological DMARDs such as anti-tumor necrosis factor (TNF) therapy [4,5]. Patients on these therapies are advised to undergo screening for tuberculosis in a timely manner. Medical practitioners stress the importance of early diagnosis and personalized treatment in preventing or minimizing joint destruction in treating RA [2] Having this as the treatment strategy for RA and coupled with frequent assessment of disease activity, patients are reported to have improved prognosis [10].
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