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WICK

Immunoendocrine communication via the hypothalamo-pituitary-adrenal axis in autoimmune diseases.

Wick G, Hu Y, Schwarz S, Kroemer G.

Endocr Rev. 1993 Oct;14(5):539-63. Review.

"The interrelationship between the neuroendocrine and the immune systems has long been a neglected subject of study. In spite of the pioneering work of the group of Besedovsky and Sorkin (l), this area was apparently deemed too suspicious of polypragmatism for most neurologists, endocrinologists, and immunologists. Only after scientists from all of these fields decided to combine their expertise, immunoendocrinology became a discipline of its own, and the last decade has experienced an explosive growth of the number of papers dealing with physiological and pathological immunoendocrine interactions. Many excellent reviews on this topic have appeared (2-5). Several of these also appeared in Endocrine Reviews, specifically some classics on the subject of the physiological and pharmacological effects of glucocorticoid hormones (GC) in stress and aging (6, 7), and also on the immunoendocrine dialogue via the hypothalamo-pituitary-adrenal (HPA) axis (8). The potential modulatory role of this feedback regulation in the pathogenesis of autoimmune disease has only been suggested recently (9-13). It is the aim of this review to summarize and discuss the present state of knowledge of alterations of the immunoendocrine circuit along the HPA axis in various autoimmune diseases in experimental animals and man. However, while most of the previous reviews cited above were mainly written from an endocrinologist’s standpoint, the present one is presented from an immunologist’s view. Therefore, a certain amount of immunological background information is always provided for the more endocrinologically oriented reader."

"Autoimmune diseases have a multifactorial pathogenesis. We have put forward the hypothesis that two sets of essential genes must be present in an individual in order for a given autoimmune disease to develop: genes coding for abnormally increased autoreactivity of the immune system and genes coding for a primary susceptibility of the target organ (in organ-specific autoimmune diseases) or target structure in general (in systemic autoimmune diseases) for the attack of the humoral and/or cellular effector mechanisms. The final outcome of a given disease then depends on additional  modulatory factors. Among the latter, steroid hormones, particularly GC, are the most prominent."

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