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: the sympathetic nervous system and the hypothalamic-pituitary-adrenal axis.
“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
In “Neural influences on disease” (page unavailable), the review says perceived threats activate the SNS and HPA axis to regulate broad transcriptional patterns in innate immune cells, and it reports increased pro-inflammatory gene expression during chronic social adversity. But it distinguishes their effects: SNS activation stimulates pro-inflammatory genes, whereas HPA activation inhibits them; increased inflammation is linked to reduced glucocorticoid signalling. The claim overstates the HPA axis’s role if it presents both pathways as directly producing a pro-inflammatory program. (LLM, conf=0.86)
Experimental — accuracy not yet measuredAlthough 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.
“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
Split into 2 atoms — 0 confirmed, 2 partially supported, 0 disputed, 0 misattributed, 0 unverifiable. Expand the claim to see per-atom verdicts.
Experimental — accuracy not yet measuredSevere childhood stressors promote the formation of a neural-immune pipeline, wherein inflammatory cytokine signaling between the brain and the periphery is markedly amplified.
“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]
The Abstract and ‘Neural influences on disease’ section describe reciprocal brain–immune signaling and report that acute stress can increase circulating pro-inflammatory cytokines. They do not establish that cytokine signaling between the brain and periphery is markedly amplified; the childhood-stressor premise is attached to a different citation. (LLM, conf=0.84)
Experimental — accuracy not yet measuredNorepinephrine modulates immune response gene transcription via stimulation of beta-adrenergic receptors.
“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
A biologically plausible pathway exists by which stressors occurring in the social environment may influence inflammatory activity.
“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 brain can modulate inflammatory activity throughout the body via SNS-related β-adrenergic signaling and HPA axis-related cortisol production.
“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
Threat perception causes the sympathetic nervous system to release noradrenaline, which mobilizes stem cells from bone marrow and activates immune gene transcription in white blood cells, organs, and tissues.
“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
Both physical and psychological processes contribute to the net effect of a given social environment on gene expression, with each mechanism activating some distinct gene modules as well as a conserved generalized response to adverse life circumstances.
“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 socially isolated individuals, up-regulated genes included inflammation-related transcripts, while down-regulated transcripts were involved in Type I interferon innate antiviral responses and antibody production.
“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]
Across diverse forms of adversity, a common 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.
“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 both leukocytes and tumors, 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.
“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]
Strong evidence supports bidirectional communication between the central nervous system and innate immunity.
“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
The sympathetic nervous system allows the CNS to steer innate immune responses between proinflammatory and antiviral phenotypes.
“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
Sleep disturbance leads to a host defense response similar to that activated by non-physical threats.
“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
Norepinephrine regulates immune response gene transcription and proinflammatory cytokine production via β-adrenergic receptors.
“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
The conserved transcriptional response to adversity (CTRA) is characterized by increased proinflammatory and reduced antiviral skewing of basal gene expression.
“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
CTRA increases an individual's risk for viral infection and inflammation-related disease.
“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
The host defense program is activated by non-physical social, symbolic, anticipated, or imagined threats.
“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
Glucocorticoid inhibition of immune response gene transcription is mediated by at least three mechanisms: promoter binding, GR-induced antiinflammatory genes inhibiting NF-κB, and protein-protein interactions antagonizing transcription.
“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
Hypocortisolimia diminishes negative feedback control of inflammatory cytokines, resulting in a persistent pro-inflammatory profile observed in adults with ELAb.
“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)”
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Watkins, L. R., & Maier, S. F. (1999) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.96.14.7710 · Cited by 250 · cited 1× · see citing works
“Inflammatory regulation of behaviour Several molecular signalling pathways have been identified to convey peripheral pro-inflammatory and antiviral signals into the brai”
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Self-citationDose-dependent effects of endotoxin on human sleep
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“and experimental analyses of repeated social threat in animal models (such as encountering an aggressive intruder”
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Self-citationComplex Systems Science in Biomedicine
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Self-citationBower, J. E., Ganz, P. A., Irwin, M. R., Arevalo, J. M. G., & Cole, S. W. (2010) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2010.09.010 · Cited by 169 · see citing works
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Self-citationGeographical genomics of human leukocyte gene expression variation in southern Morocco
Idaghdour, Y., Czika, W., Shianna, K. V., Lee, S. H., Visscher, P. M., Martin, H. C., Miclaus, K., Jadallah, S. J., Goldstein, D. B., Wolfinger, R. D., et al. (2010) · Nature Genetics · doi:10.1038/ng.495 · Cited by 151 · cited 1× · see citing works
“These include: environmentally dependent variations in the basal transcriptome of unstimulated immune cell”
BackgroundCytokine gene polymorphisms and fatigue in breast cancer survivors: Early findings
Collado-Hidalgo, A., Bower, J. E., Ganz, P. A., Irwin, M. R., & Cole, S. W. (2008) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2008.05.009 · Cited by 137 · cited 1× · see citing works
“Fatigue in breast cancer survivors is also particularly elevated among patients with IL1B , IL6 or TNF polymorphisms that cause high-level expression of the respective cytokine”
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Genome-wide transcriptional profiling linked to social class in asthma
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“People confronting long-term social adversities — such as the mortal illness of a spouse, low socio-economic status, post-traumatic stress disorder or long-term social isolation — have repeatedly been found to show increased expression of pro-inflammatory immune response genes, despite the presence of stable or elevat…”
BackgroundSelf-citationRaison, C. L., Rye, D. B., Woolwine, B. J., Vogt, G. J., Bautista, B. M., Spivey, J. R., & Miller, A. H. (2010) · Biological Psychiatry · doi:10.1016/j.biopsych.2010.04.019 · Cited by 116 · see citing works
Mitigating Cellular Inflammation in Older Adults: A Randomized Controlled Trial of Tai Chi Chih
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Self-citationSex differences in monocyte expression of IL-6: role of autonomic mechanisms
O'Connor, M., Motivala, S. J., Valladares, E. M., Olmstead, R., & Irwin, M. R. (2007) · American Journal of Physiology-Regulatory, Integrative and Comparative Physiology · doi:10.1152/ajpregu.00752.2006 · Cited by 100 · see citing works
Self-citationSleep depth and fatigue: Role of cellular inflammatory activation
Thomas, K. S., Motivala, S. J., Olmstead, R., & Irwin, M. R. (2010) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2010.07.245 · Cited by 91 · cited 1× · see citing works
“Pro-inflammatory gene expression can induce profound fatigue during waking hour”
BackgroundSelf-citationFatigue in primary Sjögren’s syndrome – A link to sickness behaviour in animals?
Harboe, E., Tjensvoll, A. B., Vefring, H. K., Gøransson, L. G., Kvaløy, J. T., & Omdal, R. (2009) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2009.06.151 · Cited by 76 · see citing works
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“In addition to the global anti-inflammatory effect of glucocorticoids, a second neural pathway mediated by the SNS allows the CNS to 'steer' innate immune responses between pro-inflammatory and antiviral programme”
BackgroundSelf-citationTumor Necrosis Factor Antagonism Normalizes Rapid Eye Movement Sleep in Alcohol Dependence
Irwin, M. R., Olmstead, R., Valladares, E. M., Breen, E. C., & Ehlers, C. L. (2009) · Biological Psychiatry · doi:10.1016/j.biopsych.2008.12.004 · Cited by 57 · cited 1× · see citing works
“TNF antagonism can also normalize REM sleep levels (for example, in abstinent alcohol-dependent individuals, who have elevated amounts of REM sleep”
BackgroundSelf-citationCho, H. J., Seeman, T. E., Bower, J. E., Kiefe, C. I., & Irwin, M. R. (2009) · Biological Psychiatry · doi:10.1016/j.biopsych.2009.06.008 · Cited by 55 · cited 1× · see citing works
“Clinical studies have documented links between inflammation-related biomarkers and the development of fatigue both in healthy older adult”
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Self-citationSleep and Immunity: Cytokine Pathways Linking Sleep and Health Outcomes
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Self-citationImmunogenic dendritic cells primed by social defeat enhance adaptive immunity to influenza A virus
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“, but recent findings suggest that this circuit originates with the innate immune syste”
BackgroundThe Complexity of Dynamic Host Networks
Cole, S. W. (2007) · Springer eBooks · doi:10.1007/978-0-387-33532-2_26 · Cited by 27 · see citing works
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The role of inflammation in depression: from evolutionary imperative to modern treatment target
Miller, A. H., & Raison, C. L. (2016) · Nature Reviews Immunology · doi:10.1038/nri.2015.5 · Cited by 3,942 · see citing works
Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206 · see citing works
“The first effector pathway that regulates systemic inflammation is the SNS.”
BackgroundInfluentialSelf-citationIrwin, M. R., Olmstead, R., & Carroll, J. E. (2016) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.05.014 · Cited by 2,085 · see citing works
“Sleep influences two primary effector systems, the hypothalamus-pituitary-adrenal axis and the sympathetic nervous system, which together shift the basal gene expression profile toward increased proinflammatory skewing (14,123).”
BackgroundSelf-citationCancer-related fatigue—mechanisms, risk factors, and treatments
Bower, J. E. (2014) · Nature Reviews Clinical Oncology · doi:10.1038/nrclinonc.2014.127 · Cited by 1,666 · see citing works
Interoception and Mental Health: A Roadmap.
Khalsa, S. S., Adolphs, R., Cameron, O. G., Critchley, H. D., Davenport, P. W., Feinstein, J. S., Feusner, J. D., Garfinkel, S. N., Lane, R. D., Mehling, W. E., et al. (2018) · Biological psychiatry. Cognitive neuroscience and neuroimaging · doi:10.1016/j.bpsc.2017.12.004 · Cited by 1,453 · see citing works
Why Sleep Is Important for Health: A Psychoneuroimmunology Perspective
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“In contrast to HPA activation, the SNS “steers” immune responses between antiviral and proinflammatory immune responses (Irwin & Cole 2011).”
BackgroundInfluentialSelf-citationNature Contact and Human Health: A Research Agenda
Frumkin, H., Bratman, G. N., Breslow, S. J., Cochran, B., Kahn Jr, P. H., Lawler, J. J., Levin, P. S., Tandon, P. S., Varanasi, U., Wolf, K. L., et al. (2017) · Environmental Health Perspectives · doi:10.1289/ehp1663 · Cited by 1,237 · see citing works
“Stress recovery and immune function mechanisms may not be distinct because of reciprocal relationships between these two physiologic systems (Irwin and Cole 2011; Nusslock and Miller 2016).”
BackgroundAstrocyte barriers to neurotoxic inflammation
Sofroniew, M. V. (2015) · Nature Reviews Neuroscience · doi:10.1038/nrn3898 · Cited by 1,202 · see citing works
Depression in sleep disturbance: A review on a bidirectional relationship, mechanisms and treatment
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Sleep and inflammation: partners in sickness and in health
Irwin, M. R. (2019) · Nature reviews. Immunology · doi:10.1038/s41577-019-0190-z · Cited by 1,088 · see citing works
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Inflammation: Depression Fans the Flames and Feasts on the Heat
Kiecolt-Glaser, J. K., Derry, H. M., & Fagundes, C. P. (2015) · American Journal of Psychiatry · doi:10.1176/appi.ajp.2015.15020152 · Cited by 844 · see citing works
“Peripherally releasedcytokines sendsignals viamolecular, cellular, and neural routes, which ultimately reach the brain and enhance CNS inflammation (2, 19, 20).”
BackgroundIntegrating neuroimmune systems in the neurobiology of depression
Wohleb, E. S., Franklin, T., Iwata, M., & Duman, R. S. (2016) · Nature Reviews Neuroscience · doi:10.1038/nrn.2016.69 · Cited by 668 · see citing works
Sofroniew, M. V. (2015) · Cold Spring Harbor Perspectives in Biology · doi:10.1101/cshperspect.a020420 · Cited by 695 · see citing works
Nusslock, R., & Miller, G. E. (2016) · Biological Psychiatry · doi:10.1016/j.biopsych.2015.05.017 · Cited by 672 · see citing works
“Even if it does not, the functional connections between these systems are likely to result in cross-sensitization (11,70), wherein larger neural threat responses, acting via the SNS and HPA axis, amplify inflammation and vice-versa.”
BackgroundInfluentialSleep health: Reciprocal regulation of sleep and innate immunity
Irwin, M. R., & Opp, M. R. (2017) · Neuropsychopharmacology · doi:10.1038/npp.2016.148 · Cited by 624 · see citing works
“…REVIEWS perivascular tissues), norepinephrine regulates immune response gene transcription and proinflammatory cytokine production via stimulation of β-adrenergic receptors (Nance and Sanders, 2007; Irwin and Cole, 2011), with some evidence suggesting that α-adrenergic signaling is also involved.”
BackgroundMethodInfluentialSelf-citationCreswell, J. D., Irwin, M. R., Burklund, L. J., Lieberman, M. D., Arevalo, J. M. G., Ma, J., Breen, E. C., & Cole, S. W. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.07.006 · Cited by 607 · see citing works
“…alter activity of the hypothalamic–pituitary–adrenal (HPA) axis or sympathetic nervous system, both of which produce stress mediators (e.g., cortisol, norepinephrine, eprinephrine) that can modulate NF-jB activity and pro-inflammatory gene expression (for reviews, Cole, 2009; Irwin and Cole, 2011).”
BackgroundSelf-citationMindfulness meditation and the immune system: a systematic review of randomized controlled trials
Black, D. S., & Slavich, G. M. (2016) · Annals of the New York Academy of Sciences · doi:10.1111/nyas.12998 · Cited by 599 · see citing works
Mechanisms and treatment of late-life depression
Alexopoulos, G. S. (2019) · Translational Psychiatry · doi:10.1038/s41398-019-0514-6 · Cited by 592 · see citing works
Eisenberger, N. I., & Cole, S. W. (2012) · Nature Neuroscience · doi:10.1038/nn.3086 · Cited by 590 · see citing works
Self-citationPowell, N. D., Sloan, E. K., Bailey, M. T., Arevalo, J. M. G., Miller, G. E., Chen, E., Kobor, M. S., Reader, B. F., Sheridan, J. F., & Cole, S. W. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1310655110 · Cited by 588 · see citing works
“These results suggest that SNS/β-adrenergic up-regulation of myelopoiesis may play a key role in mediating the proinflammatory component of the leukocyte CTRA dynamic (13, 17) and could potentially contribute to the increased risk of inflammatory disease observed in individuals confronting chronic social adversity (19…”
BackgroundResultInfluentialSelf-citationRole of sleep deprivation in immune-related disease risk and outcomes
Garbarino, S., Lanteri, P., Bragazzi, N. L., Magnavita, N., & Scoditti, E. (2021) · Communications Biology · doi:10.1038/s42003-021-02825-4 · Cited by 617 · see citing works
Sympathetic nervous system regulation of the tumour microenvironment
Cole, S. W., Nagaraja, A. S., Lutgendorf, S. K., Green, P. A., & Sood, A. K. (2015) · Nature Reviews Cancer · doi:10.1038/nrc3978 · Cited by 576 · see citing works
Self-citationThe Emerging Field of Human Social Genomics
Slavich, G. M., & Cole, S. W. (2013) · Clinical Psychological Science · doi:10.1177/2167702613478594 · Cited by 523 · see citing works
“…CTRA generally involves a shift in the leukocyte’s basal transcriptional stance so that the body is better prepared to deal with different types of microbial exposure that have historically been associated with injury in dangerous environmental conditions (Cole et al., 2011; Irwin & Cole, 2011).”
BackgroundInfluentialSelf-citationSlavich, G. M. (2020) · Annual Review of Clinical Psychology · doi:10.1146/annurev-clinpsy-032816-045159 · Cited by 502 · see citing works
“…inhibiting the proinflammatory function of NF-κB, increasing the expression of the inhibitor of NF-κB (IκB), and antagonizing proinflammatory gene transcription via protein–protein interactions between the glucocorticoid receptor and NF-κB in the nucleus of immune cells (Irwin & Cole 2011).”
BackgroundA functional genomic perspective on human well-being
Fredrickson, B. L., Grewen, K. M., Coffey, K. A., Algoe, S. B., Firestine, A. M., Arevalo, J. M. G., Ma, J., & Cole, S. W. (2013) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1305419110 · Cited by 512 · see citing works
“However, in the very different environment of contemporary human society, chronic CTRA activation by social or symbolic threats may promote inflammationmediated cardiovascular, neurodegenerative, and neoplastic diseases and impair host resistance to viral infections (12, 33, 37).”
BackgroundMethodResultInfluentialSelf-citationCole, S. W. (2014) · PLoS Genetics · doi:10.1371/journal.pgen.1004601 · Cited by 415 · see citing works
“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].”
BackgroundInfluentialSelf-citationMindfulness meditation for younger breast cancer survivors: A randomized controlled trial
Bower, J. E., Crosswell, A. D., Stanton, A. L., Crespi, C. M., Winston, D., Arevalo, J., Ma, J., Cole, S. W., & Ganz, P. A. (2015) · Cancer · doi:10.1002/cncr.29194 · Cited by 390 · see citing works
Self-citationIn Sickness and in Health: The Co-Regulation of Inflammation and Social Behavior
Eisenberger, N. I., Moieni, M., Inagaki, T. K., Muscatell, K. A., & Irwin, M. R. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.141 · Cited by 396 · see citing works
“A more detailed account of the specific mechanisms whereby social factors regulate immune system responses is presented elsewhere (Irwin and Cole, 2011; Slavich and Cole, 2013; Slavich and Irwin, 2014).”
BackgroundSelf-citationBehaviorally Assessed Sleep and Susceptibility to the Common Cold
Prather, A. A., Janicki‐Deverts, D., Hall, M. H., & Cohen, S. (2015) · SLEEP · doi:10.5665/sleep.4968 · Cited by 399 · see citing works
Slavich, G. M., & Sacher, J. (2019) · Psychopharmacology · doi:10.1007/s00213-019-05326-9 · Cited by 383 · see citing works
Mind–body therapies and control of inflammatory biology: A descriptive review
Bower, J. E., & Irwin, M. R. (2016) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2015.06.012 · Cited by 388 · see citing works
“Alterations in inflammatory processes are thought to play a role in many of the symptoms and conditions that are responsive to MBTs, including fatigue, depression, and pain (Irwin and Cole, 2011).”
BackgroundInfluentialSelf-citationSmith, K. E., & Pollak, S. D. (2020) · Perspectives on Psychological Science · doi:10.1177/1745691620920725 · Cited by 351 · see citing works
“By its nature, the innate immune system functions in a nonspecific manner, producing similar responses to many different types of challenges (Irwin & Cole, 2011; Maier & Watkins, 1998).”
BackgroundStress and cancer: mechanisms, significance and future directions
Eckerling, A., Ricon-Becker, I., Sorski, L., Sandbank, E., & Ben-Eliyahu, S. (2021) · Nature Reviews Cancer · doi:10.1038/s41568-021-00395-5 · Cited by 348 · see citing works
Psychological Stress and Mitochondria: A Systematic Review
Picard, M. A., & McEwen, B. S. (2018) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000545 · Cited by 339 · see citing works
“The resulting findings from psychosomatic medicine, psychoneuroimmunology, and psychoneuroendocrinology have demonstrated that psychosocial experiences and life exposures influence subcellular processes including immune activation/suppression (14,15), oncogenic behavior (16), gene expression regulation (17), telomere…”
BackgroundClustering of depression and inflammation in adolescents previously exposed to childhood adversity
Miller, G. E., & Cole, S. W. (2012) · Biological Psychiatry · doi:10.1016/j.biopsych.2012.02.034 · Cited by 331 · see citing works
Self-citationDisentangling the Links Between Psychosocial Stress and Cardiovascular Disease
Osborne, M. T., Shin, L. M., Mehta, N. N., Pitman, R. K., Fayad, Z. A., & Tawakol, A. A. (2020) · Circulation Cardiovascular Imaging · doi:10.1161/circimaging.120.010931 · Cited by 339 · see citing works
Social status alters immune regulation and response to infection in macaques
Snyder-Mackler, N., Sanz, J., Kohn, J. N., Brinkworth, J. F., Morrow, S., Shaver, A. O., Grenier, J.-C., Pique-Regi, R., Johnson, Z. P., Wilson, M. E., et al. (2016) · Science · doi:10.1126/science.aah3580 · Cited by 318 · see citing works
Creswell, J. D., Taren, A. A., Lindsay, E. K., Greco, C. M., Gianaros, P. J., Fairgrieve, A., Marsland, A. L., Brown, K. W., Way, B. M., Rosen, R. K., et al. (2016) · Biological Psychiatry · doi:10.1016/j.biopsych.2016.01.008 · Cited by 299 · see citing works
“Specifically, efferent projections from dlPFC might modulate medial prefrontal cortex and subcortical cell groups known to trigger peripheral stress and inflammatory response cascades (51,52).”
BackgroundCole, S. W., Capitanio, J. P., Chun, K., Arevalo, J. M. G., Ma, J., & Cacioppo, J. T. (2015) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1514249112 · Cited by 310 · see citing works
“Lonely people showed elevated SNS and hypothalamus-pituitary-adrenal–axis activity, relative expansion of the circulating monocyte pool, and monocyte-related activation of the CTRA transcriptome profile marked by upregulated expression of proinflammatory genes and downregulated expression of type I IFN- and antibody-r…”
BackgroundSelf-citationPsychological Stress and Mitochondria: A Conceptual Framework
Picard, M. A., & McEwen, B. S. (2018) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000544 · Cited by 318 · see citing works
Multiple Roles for Astrocytes as Effectors of Cytokines and Inflammatory Mediators
Sofroniew, M. V. (2014) · The Neuroscientist · doi:10.1177/1073858413504466 · Cited by 333 · see citing works
Social environment is associated with gene regulatory variation in the rhesus macaque immune system
Tung, J., Barreiro, L. B., Johnson, Z. P., Hansen, K. D., Michopoulos, V., Toufexis, D., Michelini, K., Wilson, M. E., & Gilad, Y. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1202734109 · Cited by 277 · see citing works
“For instance,NR3C1, the GC receptor gene, plays a key role in linking behavior, HPA axis-mediated stress responses, and gene expression (30).”
BackgroundResultIrwin, M. R., Olmstead, R., Carrillo, C., Sadeghi, N., Breen, E. C., Witarama, T., Yokomizo, M., Lavretsky, H., Carroll, J. E., Motivala, S. J., et al. (2014) · Sleep · doi:10.5665/sleep.4008 · Cited by 303 · see citing works
Self-citationThe Effects of Mind-Body Therapies on the Immune System: Meta-Analysis
Morgan, N., Irwin, M. R., Chung, M., & Wang, C. (2014) · PLoS ONE · doi:10.1371/journal.pone.0100903 · Cited by 294 · see citing works
“Classification of the immune outcomes for this meta-analysis was guided by functional genomics studies that have identified two broad gene expression programs that can be induced in myeloid lineage cells by different types of microbial stimulus, and that can also be regulated by stress response mechanisms [28].”
BackgroundInfluentialSelf-citationCahn, B. R., Goodman, M. S., Peterson, C. T., Maturi, R., & Mills, P. J. (2017) · Frontiers in Human Neuroscience · doi:10.3389/fnhum.2017.00315 · Cited by 292 · see citing works
“Chronic inflammatory states can be triggered through psychosocial stress (Steptoe et al., 2007; Miller et al., 2009; Irwin and Cole, 2011), and psychosomatic interventions like meditative practices that invoke stress-reduction mechanisms and psychophysiological self-regulation have demonstrated…”
BackgroundBower, J. E., Greendale, G., Crosswell, A. D., Garet, D., Sternlieb, B., Ganz, P. A., Irwin, M. R., Olmstead, R., Arevalo, J., & Cole, S. W. (2014) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2014.01.019 · Cited by 283 · see citing works
“…plays a key role in the onset and progression of a number of physical conditions, including cancer, cardiovascular disease, and diabetes (Libby and Theroux, 2005; Pierce et al., 2009), and is also linked to depression, pain, fatigue, and other behavioral disturbances (Irwin and Cole, 2011).”
InfluentialSelf-citationMayer, E. A., Labus, J. S., Tillisch, K., Cole, S. W., & Baldi, P. (2015) · Nature Reviews Gastroenterology & Hepatology · doi:10.1038/nrgastro.2015.121 · Cited by 282 · see citing works
Self-citationAutonomic dysreflexia after spinal cord injury: Systemic pathophysiology and methods of management
Eldahan, K. C., & Rabchevsky, A. G. (2017) · Autonomic Neuroscience · doi:10.1016/j.autneu.2017.05.002 · Cited by 279 · see citing works
“In intact subjects, the immune system is modulated by the hypothalamic-pituitary-adrenal axis (HPA) and sympathetic nervous system (SNS) (reviewed in Irwin and Cole, 2011).”
BackgroundSchwab, J. M., Zhang, Y., Kopp, M. A., Brommer, B., & Popovich, P. G. (2014) · Experimental Neurology · doi:10.1016/j.expneurol.2014.04.023 · Cited by 260 · see citing works
“…response evolves in parallel including potent anti-inflammatory mechanisms both within and outside the spinal cord, presumably to regulate ongoing inflammation initiated by trauma (Lucin et al., 2007, 2009; Riegger et al., 2007, 2009, for review see Irwin and Cole, 2011; Meisel et al., 2005) (Fig.”
BackgroundA Bayesian Model of Category-Specific Emotional Brain Responses
Wager, T. D., Kang, J., Johnson, T. D., Nichols, T. E., Satpute, A. B., & Barrett, L. F. (2015) · PLOS Computational Biology · doi:10.1371/journal.pcbi.1004066 · Cited by 262 · see citing works
“According to such theories, each emotion type arises from a dedicated population of neurons that are [1] architecturally separate, [2] homologous with other animals and [3] largely subcortical or paralimbic (e.”
BackgroundThe evolutionary significance of depression in Pathogen Host Defense (PATHOS-D)
Raison, C. L., & Miller, A. H. (2013) · Molecular Psychiatry · doi:10.1038/mp.2012.2 · Cited by 253 · see citing works
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“…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
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“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
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“…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 · see citing works
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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
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“We speculate that TCC induces a relaxation response, which reduces sympathetic outflow (41), with effects on inflammation (42).”
BackgroundMethodInfluentialSelf-citationSocial regulation of human gene expression: mechanisms and implications for public health
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“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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“, 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).”
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“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
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“A prevailing notion is that brain-derived neurogenic signals modulate immune functions (Irwin and Cole, 2011; Kipnis, 2016; Sternberg, 2006; Tracey, 2009).”
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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
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“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
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Sleep disturbance, inflammation and depression risk in cancer survivors
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“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?
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“, 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).”
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“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
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“…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).”
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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.”
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“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 146 · see citing works
“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”
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- 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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