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Organisms respond to a variety of environmental agents, such as those that cause inflammation, by mounting a coordinated complex series of adaptive responses involving the immune, nervous and endocrine systems. These adaptations are aimed at restoring the homeostatic balance and the return to the status quo ante. This interaction is facilitated by cytokines, hormones and neurotransmitters, as well as receptors that are endogenous to the neural, immune and endocrine systems. These shared ligands and receptors provide the molecular basis of this cross-talk. Studies of animal models of autoimmune diseases have shown that defects in the neuroendocrine immune communications contribute to the development of chronic inflammatory autoimmune disease. By analogy, similar observations have now been made in patients with inflammatory rheumatic disorders. For instance, patients with rheumatoid arthritis have abnormally low cortisol responses to inflammation, whilst the production of prolactin is excessive and dysregulated. Prolactin is a pro-inflammatory neuropeptide. This paper reviews the evidence to support the viewpoint that the neuropeptide arginine vasopressin, which is also produced by the hypothalamus, should be considered to be another neuroendocrine modulator of immune and inflammatory responses. It is also being hypothesized that the production of arginine vasopressin might be dysregulated and excessive in rheumatoid arthritis, and that this could be another additional neuroendocrine factor contributing to the pathophysiology of the disease.

Hypothalamic-pituitary-mediated immunomodulation: arginine vasopressin is a neuroendocrine immune mediator