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It has been suggested that dysregulation of the neuroendocrine system is an important pathogenetic mechanism of rheumatoid arthritis (RA). The dramatic response of patients with RA to glucocorticoids, the aggravation of RA after resection of bilateral adrenal glands, the inappropriately normal plasma cortisol levels in patients with RA, the blunted plasma cortisol responses after surgical stress, and the essential role of glucocorticoids in the development of streptococcal cell wall induced arthritis in Lewis rats provide evidence that dysregulation of the hypothalamic-pituitary-adrenal (HPA) axis or relative glucocorticoid deficiency might play a part in the development of RA.1,2 The involvement of glucocorticoids in the development of thymocytes further supports the role of glucocorticoid in autoimmune diseases like RA.3
The human glucocorticoid receptor (hGR) is a transcriptional factor …