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. 2008 Mar-Apr;252(1-2):1-6.
doi: 10.1016/j.cellimm.2008.05.006. Epub 2008 Jul 10.

Neuroendocrine interactions in the immune system

Affiliations

Neuroendocrine interactions in the immune system

Dennis D Taub. Cell Immunol. 2008 Mar-Apr.

Abstract

Substantial evidence now exists supporting the bidirectional communication between the neuroendocrine and immune systems. A number of hormonal and neuropeptide mediators have been shown to influence immune development and function in healthy, aged and diseased individuals. Immune cell subsets express receptors for many of these ligands and similarly, receptors for cytokines and growth factors have been identified on cells within the central nervous and endocrine systems. During times of stress or injury, each of these systems come into play and transmits messages to one another. The lines of communication between the immune system and these various neuronal and endocrine organ systems constitute specific axes of interactions, which have been shown to have a profound impact on immune function, disease development and susceptibility to infections and disease. In this Special Issue, experts in neuroendocrine immunology have provided comprehensive reviews on the current advances in this area of research as well as commentary on relevance of the various axes in controlling immunity and disease development.

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Conflict of interest statement

Conflict of Interest: Authors declare that there is no conflict of interest with the work

Figures

Fig. 1
Fig. 1
Neuroendocrine Interactions within the Immune System. As described in the text and within the specific reviews in this series, the crosstalk between the various neuronal and endocrine and immune systems appears to be primarily mediated via the production of and through interactions with soluble immune and neuroendocrine mediators, although there is substantial literature supporting a role for signals provided by the innervations of lymphoid tissues and other organ systems in controlling immune development and inflammation. Several hormonal and neuropeptide systems have been shown to influence immune activation and function including sex hormones (including estrogen, testosterone, GnRH), stress hormones (corticosteroids, ACTH), pituitary hormones (GH, prolactin), metabolic hormones (leptin, ghrelin, IGF-1) and opioids (enkephalins, endorphins and dynorphins) as well as the sympathetic nervous system (SNS). These mediators that provide the link between the endocrine, central nervous and immune systems and constitute specific axes of interactions including the hypothalamic-pituitary-adrenal (HPA) axis, hypothalamic–pituitary–gonadal (HPG) axis, hypothalamic– pituitary–thyroid (HPT) axis and the hypothalamic–growth-hormone axis. Immune cells, in their resting state or upon activation by specific antigens, cytokines and/or stress/injury, express cell surface receptors for these hormones and peptides permitting responses to ligands. Similarly, cells within the neuronal and endocrine systems can express receptors to various immune-derived cytokines, chemokines and growth factors. During states of physical (trauma, tissue damage, infection, inflammation, transplantation) or psychological stress, these various organ systems “come to life” and release mediators to facilitate crosstalk with each other controlling cytokine production, immune activation, cytotoxicity, thymopoiesis, hematopoiesis, etc‥ Overall, communication between these various systems appears to be multidirectional with specific hormones, peptides, cytokines and growth factors serving as mediators transmitting signals during times of stress, injury, disease, infection, physical decline and states of energy excess and deficit.

References

    1. Steinman L. Elaborate interactions between the immune and nervous systems. Nat. Immunol. 2004;5:575–581. - PubMed
    1. Butts CL, Sternberg EM. Neuroendocrine factors alter host defense by modulating immune function. Cell Immunol. 2008 - PMC - PubMed
    1. Bird MD, Karavitis J, Kovacs EJ. Sex differences and estrogen modulation of the cellular immune response after injury. Cell Immunol. 2008 - PMC - PubMed
    1. Kovats S, Carreras E. Regulation of dendritic cell differentiation and function by estrogen receptor ligands. Cell Immunol. 2008 - PMC - PubMed
    1. Pacifici R. Estrogen deficiency, T cells and bone loss. Cell Immunol. 2007 - PubMed

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