Neuroendocrine Regulation of Immunity

TLDR

The central nervous system regulates immunity through hormonal and neuronal pathways, notably the hypothalamic‑pituitary‑adrenal axis and sympathetic adrenergic signaling, with glucocorticoids acting as key effectors to modulate immune cells during stress and infection. The review aims to examine how the neuroendocrine system regulates immune responses. It details how disruptions in neuroendocrine signaling predispose to and influence immune diseases, and elucidates glucocorticoid mechanisms on immune cells and molecules. The review finds that interruptions in neuroendocrine regulation contribute to immune disease predisposition and expression, and that glucocorticoids exert specific effects on immune cells and molecules.

Abstract

A reciprocal regulation exists between the central nervous and immune systems through which the CNS signals the immune system via hormonal and neuronal pathways and the immune system signals the CNS through cytokines. The primary hormonal pathway by which the CNS regulates the immune system is the hypothalamic-pituitary-adrenal axis, through the hormones of the neuroendocrine stress response. The sympathetic nervous system regulates the function of the immune system primarily via adrenergic neurotransmitters released through neuronal routes. Neuroendocrine regulation of immune function is essential for survival during stress or infection and to modulate immune responses in inflammatory disease. Glucocorticoids are the main effector end point of this neuroendocrine system and, through the glucocorticoid receptor, have multiple effects on immune cells and molecules. This review focuses on the regulation of the immune response via the neuroendocrine system. Particular details are presented on the effects of interruptions of this regulatory loop at multiple levels in predisposition and expression of immune diseases and on mechanisms of glucocorticoid effects on immune cells and molecules.