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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
The cited source says what the claim attributes to it.
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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Glymphatic System Dysfunction in Thyroid‐Associated Ophthalmopathy: A Multimodal MRI Study
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“…in TAO patients may be influenced by a combination of neuroinflammation; pro-inflammatory cytokines can affect the hypothalamic–pituitary–adrenal axis and the limbic system, increasing the risk of depression and anxiety [46–48], while also exacerbating disruptions in the sleep–wake cycle [49].”
Zhu, Y., Chen, F., Fang, X., Liang, N., Na, G., & Liu, Z. (2025) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.120934 · Cited by 5
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“In general, activation of the sympathetic branch of the ANS leads to increased in fl ammation and activation of the parasympathetic branch leads to decreased in fl ammation (94).”
Psychological stress and myocardial extracellular matrix remodeling- a pathologic synergy
Spinale, F. G., Weil, B. R., Sharma, U. C., Wood, S. K., Hollis, F., Meléndez, G. C., DeLeon‐Pennell, K. Y., Bradshaw, A. D., Lang, J. K., Canty, J. M., et al. (2026) · Biochemical Pharmacology · doi:10.1016/j.bcp.2026.117795 · Cited by 4
Yao, L., Yan, R., & Sun, C. (2026) · Frontiers in Neuroscience · doi:10.3389/fnins.2026.1819436 · Cited by 4
Molecular aspects of regeneration and neuroprotection in neuropsychiatric diseases
Farooqui, A. A. (2020) · Elsevier eBooks · doi:10.1016/b978-0-12-821711-5.00008-5 · Cited by 2
Hemond, C. C., Deshpande, M., Morales, I. B., Zheng, S., Meyer, J. S., Slavich, G. M., & Cole, S. W. (2024) · Scientific Reports · doi:10.1038/s41598-024-62960-w · Cited by 3
Self-citationFLI1 in PBMCs contributes to elevated inflammation in combat-related posttraumatic stress disorder
Li, P., Liu, L., Liu, S., Lu, Z., Halushka, P. V., Sidles, S. J., LaRue, A. C., Wang, Z., & Fan, H. (2024) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2024.1436690 · Cited by 3
“This phenomenon suggests a link between peripheral in fl ammation, mediated by PBMCs, and neuroin fl ammation, facilitated by the activation of microglia and astrocytes through cytokine transport across the blood-brain barrier (5, 10 – 12, 36, 40).”
BackgroundGao, R., Huang, Y., Mao, S., He, H., Yao, J., Feng, J., & Wang, Y. (2025) · BMC Anesthesiology · doi:10.1186/s12871-025-02959-6 · Cited by 3
“In particular, the activation of β-adrenergic signaling induces an increase in nuclear factor κB (NF-κB), inflammatory gene expression, pro-inflammatory cytokine production, and systemic inflammatory markers [35, 36].”
Identification of Symptom Profiles in Prostate Cancer Survivors
An, J., Blair, C. K., Lin, Y., Lu, S., Arap, W., Saraiya, B., Irwin, M. R., & Kinney, A. Y. (2025) · Oncology nursing forum · doi:10.1188/25.onf.137-150 · Cited by 4
“These symptoms have also been referred to as sickness behavior, which is an adaptive response of the body to illness induced by the release of proinflammatory cytokines (Irwin & Cole, 2011; Myers, 2008).”
Self-citationDepression and Inflammation in Women With Breast Cancer: Risk and Resilience Factors
Korecki, J. R., Slavich, G. M., Ganz, P. A., Irwin, M. R., Cole, S. W., Crespi, C. M., & Bower, J. E. (2025) · Psychosomatic Medicine · doi:10.1097/psy.0000000000001398 · Cited by 3
Self-citationWorthman, C. M. (2020) · Cambridge University Press eBooks · doi:10.1017/9781108695374.007 · Cited by 3
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Sporopollenin exine capsules modulate the function of microglial cells
Li, M., Hu, B., Wu, Z., Wang, Z., Weng, J. H., Zheng, H., & Sun, L. (2023) · Biomaterials Science · doi:10.1039/d3bm01154b · Cited by 3
Zhang, G., Wang, S., Ma, P., & Pan, J. (2024) · Journal of Integrative Neuroscience · doi:10.31083/j.jin2311200 · Cited by 4
Insight of the Recent Perspectives from Psychoneuroimmunology: Stress, Nutrition and Life Quality
Seyidoğlu, N., & Aydın, C. (2024) · Integrated science · doi:10.1007/978-3-031-73061-0_9 · Cited by 3
Disordered peptide-based design of intrinsically disordered polymers for biomedical applications
Coskuner‐Weber, O., Çaylı, F. N., & Uversky, V. N. (2025) · International Journal of Polymer Analysis and Characterization · doi:10.1080/1023666x.2025.2458470 · Cited by 3
“[222] The binding can activate or inhibit pathways depending on the receptor type and ligand.”
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Muñoz‐Ortega, M. H., Cervantes‐García, D., Quintanar‐Stephano, A., Campos-Esparza, M. D. R., Lorenzana, M. G., Campos‐Rodríguez, R., Rodríguez, M. G., & Ventura‐Juárez, J. (2015) · International Journal of Morphology · doi:10.4067/s0717-95022015000100034 · Cited by 3
“…pathogenassociated molecular patterns (PAMPs) and those generated for cellular stress; recent data remark the importance of endocrine and neural signaling in the modulation of immune response, this neuroendocrine modulation has effects over adaptive and innate responses (Irwin & Cole, 2011).”
BackgroundMindfulness for the Treatment of Stress Disorders
Pallesen, K. J., Dahlgaard, J., & Fjorback, L. O. (2015) · Springer eBooks · doi:10.1007/978-3-319-22255-4_8 · Cited by 3
The Psychobiology of Attachment and the Aetiology of Disease
Kidd, T. (2015) · Springer eBooks · doi:10.1007/978-3-319-23300-0_11 · Cited by 3
Evolutionary Biology of Human Stress
Worthman, C. M. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-802652-6.00032-3 · Cited by 4
Biosimilars und der Nocebo-Effekt
Braun, J., Tsiami, S., Buehring, B., KIEFER, D. M., Andreica, I., Baraliakos, X., & Kiltz, U. (2019) · Zeitschrift für Rheumatologie · doi:10.1007/s00393-019-00729-7 · Cited by 3
“Das Phänomen der erlernten Immunantwort basiert auf 2 Phänomenen: Einerseits hängt es von der intensiven bidirektionalen Kommunikation zwischen dem zentralen Nervensystem und dem Immunsystem ab [74] und andererseits von der Fähigkeit eines Organismus, einen physiologischen Reflex über assoziative Lernprozesse (klassis…”
BackgroundPost-Traumatic Stress Disorder and DNA Methylation
Rusiecki, J. A., Uddin, M., Alexander, M. S., & Moore, L. E. (2016) · Springer eBooks · doi:10.1007/978-3-319-08359-9_98 · Cited by 3
Karrasch, S., Hitzler, M., Gumpp, A. M., Karabatsiakis, A., & Kolassa, I. (2020) · Verhaltenstherapie · doi:10.1159/000505380 · Cited by 4
Rentscher, K. E., Klopack, E. T., Crimmins, E. M., Seeman, T. E., Cole, S. W., & Carroll, J. (2022) · medRxiv · doi:10.1101/2022.06.03.22275977 · Cited by 3
“, catecholamines, glucocorticoids) that interact with receptors on the surface of cells [92].”
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“39 42 Home-based Yi Jin Bang and conventional exercise programs can be safely prescribed to people with subacromial pain syndrome, as we did not observe any intervention-related adverse events or dropouts.”
Wang, L., Fang, M., Wang, C., Li, J., Huang, S., Li, W., Zhuang, B., & Gong, S. (2024) · Medicine · doi:10.1097/md.0000000000039433 · Cited by 2
“[36] Depression produced a long-term stimulation of the neuroimmune connection, and this ongoing stimulation can alter the functioning of the immune system, making a person more susceptible to causing infections.”
Transcriptomics and psychotherapy: An integrative review
Ricon‐Becker, I., & Cole, S. W. (2024) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2024.100867 · Cited by 2
Self-citationThe role of immunity in comorbid pain and depression
Ciaramella, A., & Carli, G. (2024) · Exploration of Immunology · doi:10.37349/ei.2024.00168 · Cited by 3
Effects of Stress on Blood Pressure: A Literature Review
Oei, E. R., Sari, D. R., Setiawan, H. K., & Bestari, D. (2025) · International Journal Of Scientific Advances · doi:10.51542/ijscia.v6i1.6 · Cited by 2
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“29 However, poor sleep quality has been linked to an early decline in cortisol levels, 30 which potentially prolongs the inflammatory response.”
Liu, D., Guo, S., Tan, C., Zhang, K., Feng, Y., Bi, X., Jiang, J., Yang, W., & Wang, Y. (2025) · Reproductive Sciences · doi:10.1007/s43032-025-01849-z · Cited by 2
“…gestational diabetes mellitus risk the sympathetic nervous system), which shift the basal gene expression profile toward increased proinflammatory skewing, inducing an increase in inflammatory gene expression, production of proinflammatory cytokines and markers of systemic inflammation [55, 56].”
Wang, G., & Pan, S. (2025) · Journal of Cancer Survivorship · doi:10.1007/s11764-025-01922-1 · Cited by 3
Ridehalgh, C., Fundaun, J., & Farrell, S. F. (2025) · Musculoskeletal Science and Practice · doi:10.1016/j.msksp.2025.103468 · Cited by 2
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“Or it may increase the expression of inflammatory markers by activating the sympathetic nervous system and βadrenergic signaling, thereby activating the inflammatory response and increasing the risk of depression [46,47].”
Gurgoglione, F. L., Triglia, L. T., Dallaglio, G., Navacchi, R., Caraffini, A., Frassoni, B., Martini, C., Cicala, G., Palumbo, A. A., Gregorio, M. D., et al. (2026) · Journal of Cardiovascular Development and Disease · doi:10.3390/jcdd13050192 · Cited by 2
“From a pathophysiological perspective, the neurohumoral circuits involved in the bidirectional heart–brain interactions and with the stress-inflammation axis, may play a central role in the development of SCAD [24–26].”
The Case of "Judith": A Neuropsychologist's Perspective
Webb, N. E. (2015) · Pragmatic Case Studies in Psychotherapy · doi:10.14713/pcsp.v11i1.1886 · Cited by 1
“At the time Judith's case report was written, there were 192 peer-reviewed articles in the publicly available literature documenting the role of stress and the associated endocrine changes as a cause of depression (Irwin & Cole, 2011; Mills et al., 2013).”
BackgroundGu, S., Yuan, X., Yin, P., Li, Y., Wang, C., Gu, M., Xu, L., Gao, C., Wu, Y., Hu, Y., et al. (2024) · Frontiers in Neurology · doi:10.3389/fneur.2024.1388131 · Cited by 2
“Notably, there is a strong association between inflammation and depression (40, 41) (Figure 4).”
BackgroundTian, Y., Kong, S., Li, M., Wang, G., He, J., Lei, F., Lin, L., & Li, J. (2025) · The journal of nutrition health & aging · doi:10.1016/j.jnha.2025.100557 · Cited by 2
Substance use disorders: a call for a staging paradigm
Bachi, K., Hurd, Y. L., & Salsitz, E. A. (2025) · Translational Psychiatry · doi:10.1038/s41398-025-03484-3 · Cited by 2
Liang, J., Pan, X., Zhao, L., & Li, Y. (2025) · Nature and Science of Sleep · doi:10.2147/nss.s520079 · Cited by 3
“18 Meanwhile, inflammation may serve as a contributing factor to the development of depression.”
A Body Divided: Toward Reunification of the Paradigm
Farage, M. A. (2014) · Journal of Advances in Medicine and Medical Research · doi:10.9734/bjmmr/2014/9506 · Cited by 3
“Childhood neglect and other early life social adversity causes transcriptional modulation of the developing immune system with patterns of enhanced inflammatory gene expression and inhibited antiviral gene expression; for example, social distress perceived by the CNS influences transcription decision-making in leukocy…”
BackgroundNEW INSIGHTS INTO THE FUNCTION AND DEVELOPMENT OF THE SOLDIER CASTE IN TERMITES
Tian, L. (2015) · UKnowledge (University of Kentucky) · Cited by 2
Pecceu, E., Stebbing, B., Pereira, Y. M., Handel, I. G., Culshaw, G., Hodgkiss‐Geere, H., & Lawrence, J. (2017) · Veterinary Research Communications · doi:10.1007/s11259-017-9695-8 · Cited by 2
“…which tumourmediated inflammation triggers vagal afferent traffic to the brain to modulate immune and neuroendocrine function (Tracey 2002; Gidron et al. 2005; Mravec et al. 2006; Gidron and Ronson 2008; Golan et al. 2009; Rosas-Ballina and Tracey 2009; Irwin and Cole 2011; Olofsson et al. 2012).”
BackgroundCapturing Context Is Not Enough
Lemelson, R., & Tucker, A. (2020) · Cambridge University Press eBooks · doi:10.1017/9781108695374.023 · Cited by 2
King, C. D., Boggero, I. A., Schulert, G. S., Pickerill, H. M., & Cole, S. W. (2021) · PAIN Reports · doi:10.1097/pr9.0000000000000874 · Cited by 2
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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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