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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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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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