The Neuroendocrine-Immune Interface

Abstract

In an era of increased specialization where the trend has been for the individual scientist to delve ever deeper into smaller pools effectively knowing more and more about less and less, one area of research in particular has bucked the trend. The increasing interest in the bidirectional interactions of the immune and the neuroendocrine systems, and the importance of these systems in relation to sickness, inflammation, and immune-mediated diseases has required a sea change to this reductionist approach. Susceptibility to a number of autoimmune diseases, such as rheumatoid arthritis (RA) and multiple sclerosis (MS), have clear genetic components. However, it is also evident that not all individuals with a genetic predisposition go on to develop these diseases, nor is the disease of equal severity in all individuals. The question of which factors may be responsible in increasing susceptibility to and/or the severity of disease have implicated a whole host of neuroendocrine factors. The anti-inflammatory effects of the glucocorticoids released from the adrenal cortex are well established, and the role of the hypothalamo-pituitary-adrenal (HPA) axis in controlling the release of the glucocorticoids has been of considerable research interest. A proinflammatory role has been proposed for prolactin, which is itself under the positive control of other hormones released from the hypothalamus. Growth hormone has been similarly implicated. The major gender differences associated with many autoimmune diseases have implicated the gonadal steroids.