THE PATHOGENESIS OF RHEUMATOID ARTHRITIS: FROM MOLECULES TO THE WHOLE PATIENT

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Abstract
The pathogenesis of RA has now been worked out in considerable detail. The cell types involved have been characterized: monocyte/macrophages, T and B cells, synoviocytes and endothelial cells. The processes which are involved include cell adhesion and migration, T and B cell activation, cytokine release and joint destruction. The molecules which participate in these complex interactions have, for the most part, been cloned and sequenced and the function of their products studied intensively. However, despite the knowledge gathered by this reductionist approach we still do not understand fully the pathogenesis of the disease. This problem is resolvable by considering the fact that the synovitis is taking place within an individual in whom a number of other complex systems are interacting with the immune system. Of these, the neu-roendocrine system is probably one of the most important as it has the ability to downregulate inflammation through the secretion of cortisol. Study of the hypothalamic—pituitary—adrenal axis in patients with RA has shown that it responds poorly to inflammatory stimuli. This defect may not only be an important factor in determining the severity of joint inflammation but could be an important early event in the switch from acute to joint inflammation. These findings reinforce the belief that exciting and high quality clinical research is still of crucial importance in our understanding of complex biological processes such as RA.

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