Functionally polarised CD4-positive T-cell responses based on their profile of cytokine secretion are seen in many chronic autoimmune inflammatory diseases. The focus in this review is the disease-triggering role of a T-helper subset of lymphocytes.
Rheumatoid arthritis (RA) is a chronic autoimmune inflammatory and systemic disease characterised by long-term chronic synovial inflammation, hyperplasia and joint damage. Systemic features of RA include cardiovascular complications, pulmonary complications and skeletal disorder.1 According to the National Rheumatoid Arthritis Society (NRAS), there are about 690,000 adults living in the UK with the condition. The disease is more common in the 40–60 age group, and NRAS suggests that the condition is three times more common in women. Thus, it seems critical to understand the underlying pathophysiological mechanisms behind RA in order to design better treatment strategies.
Despite of intense study and research, the pathogenesis of RA remains unclear. Numerous hypotheses have been proposed to unravel the mystery behind the development of RA, but none has completely illustrated the cause that underlies the slow, progressive and chronic inflammatory response in the joints that ultimately leads to joint damage and severe disability. Several studies report that T cells are the major culprit in initiating the detrimental inflammatory response in the joints. In addition, the role of the humoral immune response is seen as equally important in autoimmune RA, where antibodies (rheumatoid factor [RF]) are generated against the healthy joint tissue. Over the long term, these antibodies damage the tissue of the joints, leading to the pathological condition in RA. Several studies have suggested that RA is triggered by genetic, environmental, epigenetic and dietary factors,1 as shown in Figure 1.
The exact pathophysiological mechanism of RA is not fully understood; however, the most accepted hypothesis is the inflammatory response mediated by humoral and cell-mediated immune response.1 The role of IgG autoantibodies and immune complexes has been recognised as a potent pathological trigger of inflammatory response, and autoantibodies (RF) are detected in more than 80% of RA patients.2 These antibodies consistently erode the lining of the joints, producing inflammation of the synovium and the symptoms associated with RA.2
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