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Reciprocal regulation of the neural and innate immune systems
Open accessAbstract
Innate immune responses are regulated by microorganisms and cell death, as well as by a third class of stress signal from the nervous and endocrine systems. The innate immune system also feeds back, through the production of cytokines, to regulate the function of the central nervous system (CNS), and this has effects on behaviour. These signals provide an extrinsic regulatory circuit that links physiological, social and environmental conditions, as perceived by the CNS, with transcriptional 'decision-making' in leukocytes. CNS-mediated regulation of innate immune responses optimizes total organism fitness and provides new opportunities for therapeutic control of chronic infectious, inflammatory and neuropsychiatric diseases.
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“Two physiological pathways are responsible for converting social-environmental adversity into broad proinflammatory transcriptional programs such as the CTRA.”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Irwin & Cole, 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“Although these regions do not directly regulate inflammatory activity, they have anatomical connections to lower level brain regions, including the hypothalamus and brainstem autonomic control nuclei, which influence systemic inflammation by modulating the activity of the HPA axis and SNS”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Irwin & Cole, 2011
Experimental — accuracy not yet measuredThe source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
In the citing paper
“This hypothesis grows out of mounting evidence that severe childhood stressors promote the formation of a neural-immune pipeline (15), wherein inflammatory cytokine signaling between the brain and the periphery is markedly amplified (16).”
From Clustering of depression and inflammation in adolescents previously exposed to childhood adversity (2012) · cites this paper as [16]
Experimental — accuracy not yet measuredThe cited source says what the claim attributes to it.
In the citing paper
“Once released, norepinephrine modulates immune response gene transcription via stimulation of β -adrenergic receptors”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Irwin & Cole, 2011
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In the citing paper
“a biologically plausible pathway exists by which stressors occurring in the social environment may influence inflammatory activity”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Irwin & Cole, 2011
The cited source says what the claim attributes to it.
In the citing paper
“the brain can modulate inflammatory activity throughout the body via the processes described earlier -namely, SNS-related β -adrenergic signaling and HPA axis-related cortisol production”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Irwin & Cole, 2011
In the citing paper
“When threat is perceived, the SNS releases noradrenaline, which promotes mobilization of stem cells from the bone marrow and activates immune gene transcription within white blood cells, organs, and tissues (Irwin and Cole, 2011).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“Parallel studies on the transcriptional correlates of social disparities in health subsequently suggested that both physical and psychological processes contribute to the net effect of a given social environment, with each mechanism activating some distinct gene modules as well as a conserved generalized response to adverse life circumstances (Figure 1) [3], [5], [12].”
From Human Social Genomics (2014) · cites this paper as [5]
In the citing paper
“Genes up-regulated in socially isolated individuals included a set of transcripts that play a central role in inflammation (e.g., IL1B, IL8, PTGS2), whereas down-regulated transcripts were involved in Type I interferon innate antiviral responses (e.g., ISG, IFI, MX, and OAS family genes) and in antibody production (e.g., IGL, IGH, IGJ, and IGK) [5], [14], [15].”
From Human Social Genomics (2014) · cites this paper as [5]
In the citing paper
“Across these diverse forms of adversity, a common pattern of conserved transcriptional response to adversity (CTRA) has emerged, including increased expression of proinflammatory genes and decreased expression of genes involved in Type I interferon innate antiviral responses and IgG antibody synthesis [3], [5], [28].”
From Human Social Genomics (2014) · cites this paper as [5]
In the citing paper
“In both, chronic threat and SNS signaling activate tissue-specific transcriptional defense programs that enhance organismic mobility and prime wound healing and antimicrobial responses to tissue injury [3], [5], [36].”
From Human Social Genomics (2014) · cites this paper as [5]
In the citing paper
“substantial evidence demonstrates a reciprocal relationship between the CNS and innate immunity (Dantzer et al, 2008(Dantzer et al, , 2012;;Irwin and Cole, 2011).”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“the SNS allows the CNS to 'steer' innate immune responses between proinflammatory and antiviral phenotypes”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“with evidence that sleep disturbance leads to a similar response”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“norepinephrine regulates immune response gene transcription and proinflammatory cytokine production via stimulation of β-adrenergic receptors”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“the conserved transcriptional response to adversity (CTRA), and is characterized by increased proinflammatory and reduced antiviral skewing of the basal gene expression profile”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“which increases an individual's risk for both viral infection and inflammation-related disease”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“the host defense program is activated by non-physical social, symbolic, anticipated, or imagined threats”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“The inhibitory effects of glucocorticoid activation on immune response gene transcription is mediated by at least three mechanisms.”
From Sleep health: Reciprocal regulation of sleep and innate immunity (2017) · cites this paper as Irwin and Cole, 2011
In the citing paper
“Furthermore, hypocortisolimia diminishes negative feedback control of inflammatory cytokines, resulting in the persistent pro-inflammatory profile that is observed in adults with ELAb.(76,77)”
In the citing paper
“In what neuroimmunologist Stephen Cole refers to as the Conserved Transcriptional Response to Adversity (CTRA), increased chronic social adversity is associated with white blood cells amplifying transcription and expression of proinflammatory cytokines (Irwin & Cole, 2011).”
From On race, human variation, and who gets and dies of sepsis (2022) · cites this paper as Irwin & Cole, 2011
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Black, D. S., Cole, S. W., Irwin, M. R., Breen, E., St. Cyr, N. M., Nazarian, N., Khalsa, D. S., & Lavretsky, H. (2013) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2012.06.011 · Cited by 249
“…literature regarding the general biological characteristics of gene modules regulated in association with social adversity (i.e., upregulation of pro-inflammatory signaling pathways and downregulation of antiviral pathways) (Schultz et al., 2007; Rohleder et al., 2009; Irwin and Cole, 2011).”
BackgroundInfluentialSelf-citationCognitive-Behavioral Stress Management Reverses Anxiety-Related Leukocyte Transcriptional Dynamics
Antoni, M. H., Lutgendorf, S. K., Blomberg, B., Carver, C. S., Lechner, S., Diaz, A., Stagl, J., Arevalo, J. M. G., & Cole, S. W. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2011.10.007 · Cited by 251
“These findings provide a molecular framework for understanding the impact of behaviorally targeted interventions on human immune function, and they begin the process of mapping specific biological pathways by which those dynamics might potentially alter the course of somatic diseases such as breast cancer (56,57) and…”
BackgroundInfluentialSelf-citationSpinal cord stimulation in chronic pain: evidence and theory for mechanisms of action
Caylor, J. R., Reddy, R. D., Yin, S., Cui, C. L., Huang, M., Huang, C. W., Rao, R., Baker, D. G., Simmons, A. N., Souza, D., et al. (2019) · Bioelectronic Medicine · doi:10.1186/s42234-019-0023-1 · Cited by 251
“…cord are not likely to directly modulate systemic effects of cytokines levels, however indirect attenuation of pain, changes in mood, or improvement in sleep may result in these observed anti-inflammatory effects (Lerman et al., 2016; Irwin et al., 2006; Irwin & Cole, 2011; Slavich & Irwin, 2014).”
BackgroundMuscatell, K. A., Dedovic, K., Slavich, G. M., Jarcho, M. R., Breen, E. C., Bower, J. E., Irwin, M. R., & Eisenberger, N. I. (2015) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2014.06.201 · Cited by 240
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“Another major element of HPA and SNS activation is that these signals are relayed to the immune system (Irwin and Cole, 2011; Wohleb and Godbout, 2013).”
BackgroundIntegrated Neurobiology of Bipolar Disorder
Maletic, V., & Raison, C. L. (2014) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2014.00098 · Cited by 236
Brommer, B., Engel, O., Kopp, M. A., Watzlawick, R., Müller, S., Prüß, H., Chen, Y., DeVivo, M. J., Finkenstaedt, F. W., Dirnagl, U., et al. (2016) · Brain · doi:10.1093/brain/awv375 · Cited by 231
“Spinal cord injury-induced immune deficiency syndrome enhances infection susceptibility dependent on lesion level”
BackgroundIrwin, M. R., Olmstead, R., Breen, E. C., Witarama, T., Carrillo, C., Sadeghi, N., Arevalo, J. M. G., Ma, J., Nicassio, P., Bootzin, R., et al. (2015) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.01.010 · Cited by 227
“We speculate that TCC induces a relaxation response, which reduces sympathetic outflow (41), with effects on inflammation (42).”
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Cole, S. W. (2013) · American Journal of Public Health · doi:10.2105/ajph.2012.301183 · Cited by 225
“pro-inflammatory gene responses and decreased signaling by interferon regulatory factor family transcription factors in the decreased antiviral gene component.(30,31,42) Promoter-based bioinformatics have also revealed some more surprising differences”
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“, low mood, fatigue, and anhedonia (27)].”
Napping: a public health issue. From epidemiological to laboratory studies
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“These pathways have been described in great detail elsewhere (e.g., Graham et al., 2006; Irwin & Cole, 2011; Lupien et al., 2009; McEwen, 1998; G. Miller, Chen, & Cole, 2009; Slavich & Cole, 2013; Slavich & Irwin, 2014).”
BackgroundTranscriptional modulation of the developing immune system by early life social adversity
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“To determine whether such dynamics might be structured by social signal transduction pathways involving the SNS and the HPA axis (10, 13, 17, 32, 44), TELiS analyses also examine motifs associated with the CREB transcription factors involved in β-adrenergic signaling by SNS catecholamines and glucocorticoid response e…”
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Eisenberger, N. I. (2013) · Psychosomatic Medicine · doi:10.1097/psy.0b013e31829de2e7 · Cited by 230
Psychological well‐being and the human conserved transcriptional response to adversity
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“, IGJ) [1–3].”
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“Tai Chi may elicit behavioral responses by activating neuroendocrine and autonomic functioning and navigating neurochemical and analgesic pathways, which in turn may modulate the inflammatory response of the immune system and modify susceptibility to chronic pain (38, 39).”
BackgroundKuhlman, K. R., Chiang, J. J., Horn, S., & Bower, J. E. (2017) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2017.05.020 · Cited by 208
“When threat is perceived, the SNS releases noradrenaline, which promotes mobilization of stem cells from the bone marrow and activates immune gene transcription within white blood cells, organs, and tissues (Irwin and Cole, 2011).”
Brain Ischemia Suppresses Immunity in the Periphery and Brain via Different Neurogenic Innervations
Liu, Q., Jin, W.-N., Liu, Y., Shi, K., Sun, H., Zhang, F., Zhang, C., Gonzales, R. J., Sheth, K. N., Cava, A. L., et al. (2017) · Immunity · doi:10.1016/j.immuni.2017.02.015 · Cited by 209
“A prevailing notion is that brain-derived neurogenic signals modulate immune functions (Irwin and Cole, 2011; Kipnis, 2016; Sternberg, 2006; Tracey, 2009).”
Bower, J. E. (2019) · Cancer · doi:10.1002/cncr.31790 · Cited by 219
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“These effects are associated with increased activity of pro-inflammatory NF-kB (nuclear factor kappa-light-chain-enhancer of activated B cells) and STAT (signal transduction and transcription) family transcription factors [21], as well as EGR(early growth response) and MEF(myocyte enhance factor) and MZF (myeloid zinc…”
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“, C-reactive protein [CRP] and Interleukin-6 [IL-6]) predict body mass gain in older adults [23] and type 2 diabetes [24].”
BackgroundAutonomic Dysreflexia Causes Chronic Immune Suppression after Spinal Cord Injury
Zhang, Y., Guan, Z., Reader, B. F., Shawler, T. M., Mandrekar-Colucci, S., Huang, K., Weil, Z. M., Bratasz, A., Wells, J., Powell, N. D., et al. (2013) · Journal of Neuroscience · doi:10.1523/jneurosci.1974-13.2013 · Cited by 185
“The hypothalamic-pituitary-adrenal axis and sympathetic nervous system are key regulators of immune function (Irwin and Cole, 2011).”
BackgroundStress and asthma: Novel insights on genetic, epigenetic, and immunologic mechanisms
Rosenberg, S. L., Miller, G. E., Brehm, J. M., & Celedón, J. C. (2014) · Journal of Allergy and Clinical Immunology · doi:10.1016/j.jaci.2014.07.005 · Cited by 183
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“0–10 327 (74) 314 (76) 13 (43) 11–99 60 (14) 51 (12) 9 (30) $100 57 (13) 49 (12) 8 (27) History of cancer 427 (84) 403 (86) 24 (60) <0.”
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Sleep disturbance, inflammation and depression risk in cancer survivors
Irwin, M. R., Olmstead, R. E., Ganz, P. A., & Haque, R. (2013) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2012.05.002 · Cited by 173
“Several other behavioral interventions have been found to modulate inflammatory signaling in the innate immune system including aerobic exercise (Nicklas et al., 2008), compassion meditation (Pace et al., 2009) and Tai Chi (Irwin and Olmstead, 2011; Lavretsky et al., 2011) in association in improvements in sleep distu…”
BackgroundInfluentialSelf-citationAre social isolation and loneliness associated with cognitive decline in ageing?
Cardona, M., & Andrés, P. (2023) · Frontiers in Aging Neuroscience · doi:10.3389/fnagi.2023.1075563 · Cited by 197
“, 2007), indicating an upregulation of inflammatory signaling that can be a precursor for higher systemic inflammation (Irwin and Cole, 2011; Ligthart et al., 2018) and worse health (Slavich and Cole, 2013).”
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The role of depressive subtypes within the neuroinflammation hypothesis of major depressive disorder
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Nerve Stimulation: Immunomodulation and Control of Inflammation
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“The GRs homodimerize and transactivate anti-inflammatory cytokines such as IL-4 and IL-10.”
BackgroundInfluentialStress-induced biological aging: A review and guide for research priorities
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“Drawing on these insights, researchers have begun elucidating how chronic stress affects inflammation and its regulation by the immune, nervous, and endocrine systems (Irwin and Cole, 2011; Raison et al., 2006; Sternberg, 2006).”
Self-citationHostinar, C. E., Lachman, M. E., Mroczek, D. K., Seeman, T. E., & Miller, G. E. (2015) · Developmental Psychology · doi:10.1037/dev0000049 · Cited by 167
“Norepinephrine then accentuates inflammation by changing patterns of cell trafficking and cytokine release (Elenkov, Wilder, Chrousos, & Vizi, 2000; Irwin & Cole, 2011; Nance & Sanders, 2007).”
BackgroundResultInfluentialDepression and Insomnia in Cancer: Prevalence, Risk Factors, and Effects on Cancer Outcomes
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Self-citationNew insights into the cell- and tissue-specificity of glucocorticoid actions
Quatrini, L., & Ugolini, S. (2020) · Cellular and Molecular Immunology · doi:10.1038/s41423-020-00526-2 · Cited by 174
Irwin, M. R., Witarama, T., Caudill, M. M., Olmstead, R., & Breen, E. C. (2014) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2014.09.017 · Cited by 168
“…found that PSD induces increases in sympathoadrenal activity on awakening (Irwin and Ziegler, 2005), and such adrenergic signaling is known to increase the expression of inflammatory response genes (Irwin and Cole, 2011), possibly by activation of NF-jB (Bierhaus et al., 2003; Pace et al., 2006).”
BackgroundSelf-citationIrwin, M. R., Olmstead, R., Breen, E. C., Witarama, T., Carrillo, C., Sadeghi, N., Arevalo, J. M. G., Ma, J., Nicassio, P. M., Ganz, P. A., et al. (2014) · JNCI Monographs · doi:10.1093/jncimonographs/lgu028 · Cited by 168
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Dysregulation of inflammation, neurobiology, and cognitive function in PTSD: an integrative review
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Neuroinflammation in suicide: Toward a comprehensive model
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“Downstream biological consequences include HPA axis upregulation and increased infl ammatory response (Raison and Miller 2003; Slavich et al. 2009; Irwin and Cole 2011; Murphy et al. 2013).”
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“Neuroendocrine-immune interactions play an important role in these regulatory processes, but the mechanisms involved remain unclear 2, 3.”
Andersson, N. W., Goodwin, R. D., Okkels, N., Gustafsson, L. N., Taha, F., Cole, S. W., & Munk-Jørgensen, P. (2016) · International Journal of Epidemiology · doi:10.1093/ije/dyv333 · Cited by 139
“By triggering neuroendocrine stress-signalling pathways (such as the sympathetic nervous system and hypothalamic-pituitary-adrenal axis), which regulate multiple internal physiological processes including broad patterns of transcriptional activity in cells of the immune system, depression may potentially affect the st…”
BackgroundSelf-citationInnate immunity as a target for acute cardioprotection
Zuurbier, C. J., Abbate, A., Cabrera-Fuentes, H. A., Cohen, M. V., Collino, M., de Kleijn, D. P. V., Downey, J. M., Pagliaro, P., Preissner, K. T., Takahashi, M., et al. (2018) · Cardiovascular Research · doi:10.1093/cvr/cvy304 · Cited by 149
“hypothalamic–pituitary–adrenal axis produces glucocorticoids, which circulate throughout the body and can alter a variety of processes, including immune response gene programmes.(127) Furthermore, adrenaline”
BackgroundSavitz, J. B., Price, J. L., & Drevets, W. C. (2014) · Neuroscience & Biobehavioral Reviews · doi:10.1016/j.neubiorev.2014.02.008 · Cited by 145
Metadata
- Authors
- Irwin, M. R., & Cole, S. W.
- Affiliations
- University of California, Los Angeles (US)
- Corresponding author
- Irwin, Michael R.
- ORCID
- Irwin, Michael R.
- Venue
- Nature Reviews Immunology
- Published
- 2011-08-05
- Volume
- 11
- Issue
- 9
- Pages
- 625-632
- ISSN
- 1474-1733 (ISSN-L)
- 1474-1741
- PMC
- PMC3597082
- OpenAlex
- W2078619626
- Cited by
- 910
- References
- 85
- Citations by year
- 2026: 48 · 2025: 82 · 2024: 61 · 2023: 65 · 2022: 69 · 2021: 82 · 2020: 109 · 2019: 71 · 2018: 46 · 2017: 51 · 2016: 57 · 2015: 59 · 2014: 46 · 2013: 34 · 2012: 26
- FWCI
- 1.80
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Licence
- www.springer.com/tdm (tdm)
- Locations
- Nature reviews. Immunology (publishedVersion)
- PubMed (publishedVersion)
- Europe PMC (PubMed Central) (acceptedVersion)
- PubMed Central (acceptedVersion)
- Funders
- Science Foundation Ireland
- National Institutes of Health (1ul1rr033176-01, UL1TR000124)
- National Institute on Aging (R01AG026364, R01AG034588, R37AG033590, P30AG028748, R01AG033590)
- National Heart, Lung, and Blood Institute (R01HL079955)
- National Institute of Mental Health (R01MH091352)
- National Institute on Drug Abuse (F31DA024904)
- National Cancer Institute (R01CA116778, R21CA138687, R01CA119159)
- National Center for Research Resources (UL1-RR-033176)
- National Center for Advancing Translational Sciences
- Topics
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Neurology › Neuroinflammation and Neurodegeneration Mechanisms
- Keywords
- neuroimmune interactions, innate immunity, behavior, cytokines, stress, infection, neuropsychiatric disorders, chronic inflammation, chronic infection
- MeSH terms
- Central Nervous System, Endocrine System, Genes, MHC Class II, Humans, Immunity, Innate, Inflammation, Leukocytes, Neuroimmunomodulation, Signal Transduction, Cytokines
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