Protein hormones and immunity

Abstract

A number of observations and discoveries over the past 20 years support the concept of important physiological interactions between the endocrine and immune systems. The best known pathway for transmission of information from the immune system to the neuroendocrine system is humoral in the form of cytokines, although neural transmission via the afferent vagus is well documented also. In the other direction, efferent signals from the nervous system to the immune system are conveyed by both the neuroendocrine and autonomic nervous systems. Communication is possible because the nervous and immune systems share a common biochemical language involving shared ligands and receptors, including neurotransmitters, neuropeptides, growth factors, neuroendocrine hormones and cytokines. This means that the brain functions as an immune-regulating organ participating in immune responses. A great deal of evidence has accumulated and confirmed that hormones secreted by the neuroendocrine system play an important role in communication and regulation of the cells of the immune system. Among protein hormones, this has been most clearly documented for prolactin (PRL), growth hormone (GH), and insulin-like growth factor-1 (IGF-I), but significant influences on immunity by thyroid stimulating hormone (TSH) have also been demonstrated. Here we review evidence obtained during the past 20 years to clearly demonstrate that neuroendocrine protein hormones influence immunity and that immune processes affect the neuroendocrine system. New findings highlight a previously undiscovered route of communication between the immune and endocrine systems that is now known to occur at the cellular level. This communication system is activated when inflammatory processes induced by proinflammatory cytokines antagonize the function of a variety of hormones, which then causes endocrine resistance in both the periphery and brain. Homeostasis during inflammation is achieved by a balance between cytokines and endocrine hormones.

Inflammation and mortality in a frail mouse model

“…For example, TNF-α and IL-6 induce IGF-1 resistance in neurons and muscle cells (Kelley 2004;Kelley et al 2007). While the molecular mechanism mediating inflammationneuroendocrine interaction is not known, the activation of the IL-6 modulated JAK-STAT-SOCS pathway may be involved (Bodell et al 2009;Haddad et al 2005).…”

Insulin‐like growth factor I messenger RNA and protein are expressed in the human lymph node and distinctly confined to subtypes of macrophages, antigen‐presenting cells, lymphocytes and endothelial cells

“…Thereafter, experience from Snell dwarf mice, which carry defects in GH, prolactin, thyroid hormones and IGF-I production, and from GH-deficient humans, led to the hypothesis that the whole GH/IGF-I axis may be involved (reviewed previously). 11,12 Since then, numerous indications have been found that IGF-I plays a role in the proliferation and differentiation of lymphatic cells and tissues (reviewed previously 1,[12][13][14][15][16][17] ). For instance, in human T-lymphoblast cell lines the stimulatory action of GH on colony formation was attributed to a local production of IGF-I.…”

Clinically feasible approaches to potentiating cancer cell-based immunotherapies

“…With special reference to protein hormones, this idea has been well documented for prolactin (PRL), growth hormone (GH), and insulin-like growth factor-1 (IGF-I). 89 Unfortunately, the effects of these hormones on cancer vaccine-induced immune responses remain unexplored.…”