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Neuroimmune Regulation in Immunocompetence, Acute Illness, and Healing


Address for correspondence: Dr. Istvan Berczi, Department of Immunology, Faculty of Medicine, The University of Manitoba, 745 Bannatyne Avenue, Winnepeg, MB, R3E, 0J9, Canada. Voice: 204-789-3320; fax: 204-789-3921.


Adaptive immunocompetence is maintained by growth hormone (GH), prolactin (PRL), and vasopressin (VP). Innate or natural immunocompetence depends on cytokines, hormones (especially of the hypothalamus–pituitary–adrenal axis), and catecholamines. The acute phase response (APR, or acute febrile illness) is an emergency defense reaction whereby the adaptive, T cell–dependent, immune reactions are suppressed and the innate immune function is dramatically amplified. Infection and various forms of injury induce APR. Cytokines [interleukin (IL)-1β, tumor necrosis factor-α, and IL-6] stimulate corticotropin-releasing hormone (CRH) and VP secretion and cause a “sympathetic outflow.” Colony-stimulating factors activate leukocytes. CRH is a powerful activator of the pituitary adrenocortical axis and elevates glucocorticoid (GC) levels. Cytokines, GCs, and catecholamines play fundamental roles in the amplification of natural immune defense mechanisms. VP supports the APR at this stage. However, VP remains active and is elevated for a longer period than is CRH. VP, but not CRH, is elevated during chronic inflammatory diseases. VP controls adaptive immune function and stimulates adrenocorticotropic hormone (ACTH) and PRL secretion. PRL maintains the function of the thymus and of the T cell–dependent adaptive immune system. The ACTH–adrenal axis stimulates natural immunity and of suppressor/regulatory T cells, which suppress the adaptive immune system. VP also has a direct effect on lymphoid cells, the significance of which remains to be elucidated. It is suggested that VP regulates the process of recovery from acute illness.