Protein hormones and immunity
Open accessAbstract
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.
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Basophils and eosinophils were not found to be affected by sleep.
“As for granulocyte subsets, basophils and eosinophils were not found to be affected by sleep (67, 152, 287, 338, 480, 580).”
From The Sleep-Immune Crosstalk in Health and Disease (2019) · cites this paper as [287]
Transgenic mice overexpressing growth hormone or its receptor exhibit overgrowth of the thymus and spleen and display increases in mitogenic responses to Concanavalin A.
“Transgenic mice overexpressing growth hormone or its receptor exhibit overgrowth of the thymus and spleen and display increases in mitogenic responses to Concanavalin A [120].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [120]
Growth hormone primes neutrophils for production of lysosomal enzymes and superoxide anions, supports survival of memory T cells, increases immunoglobulin secretion of B cells, and stimulates thymulin secretion by thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst, and killing capacity of neutrophils or macrophages.
“Furthermore, growth hormone primes neutrophils for production of lysosomal enzymes and superoxide anions, supports survival of memory T cells, increases immunoglobulin secretion of B cells, and stimulates thymulin secretion by thymic epithelial cells, natural killer cell activity, phagocytosis, oxidative burst, and killing capacity of neutrophils or macrophages [120].”
From Interaction of the endocrine system with inflammation: a function of energy and volume regulation (2014) · cites this paper as [120]
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The Sleep-Immune Crosstalk in Health and Disease
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- Authors
- Kelley, K. W., Weigent, D. A., & Kooijman, R.
- Affiliations
- University of Illinois Urbana-Champaign (US)
- University of Alabama at Birmingham (US)
- Université Libre de Bruxelles (BE)
- Corresponding author
- Kelley, Keith W.
- Venue
- Brain, Behavior, and Immunity
- Publisher
- Elsevier BV
- Published
- 2007-05
- Volume
- 21
- Issue
- 4
- Pages
- 384-392
- ISSN
- 0889-1591 (ISSN-L)
- PMC
- PMC1894894
- OpenAlex
- W2025434317
- Cited by
- 217
- References
- 64
- Citations by year
- 2026: 2 · 2025: 5 · 2024: 9 · 2023: 3 · 2022: 4 · 2021: 6 · 2020: 10 · 2019: 5 · 2018: 5 · 2017: 11 · 2016: 13 · 2015: 8 · 2014: 13 · 2013: 21 · 2012: 19
- FWCI
- 6.88
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Brain Behavior and Immunity (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- VUBIR (Vrije Universiteit Brussel) (submittedVersion)
- Funders
- National Institute of Mental Health (R01MH051569, MH51569)
- National Institute of Allergy and Infectious Diseases (R01AI050442, R01AI041651, AI50442, AI41651)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Neuropeptides and Animal Physiology
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- neuroendocrine-immune interaction, protein hormones, neuroendocrine hormones, prolactin, growth hormone, insulin-like growth factor I, thyroid-stimulating hormone, cytokines, endocrine therapy resistance, inflammation, vagus nerve, neuropeptides, growth factors, neurotransmitters, immune regulation
- MeSH terms
- Animals, Humans, Insulin-Like Growth Factor I, Neurosecretory Systems, Prolactin, Psychoneuroimmunology, Growth Hormone, Neuroimmunomodulation, Receptors, Cytokine
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