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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 source backs part of the claim, not all of it — or backs it for a different population, condition or comparison.
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
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)”
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Citations
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“Following prolonged stimulation of these connections, the immune system may become dysregulated, contributing to the development and progression of autoimmune pathologies (Kiecolt-Glaser & Glaser, 2002; Glaser & Kiecolt-Glaser, 2005; Miller et al. 2009; Irwin & Cole, 2011; Voinov et al. 2013).”
BackgroundSelf-citationSuzuki, H., Savitz, J. B., Teague, T. K., Gandhapudi, S. K., Tan, C., Misaki, M., McKinney, B. A., Irwin, M. R., Drevets, W. C., & Bodurka, J. (2017) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2017.06.011 · Cited by 96
“This impairment in the adaptive immune response is hypothesized to be mediated by the suppressive effects of cortisol on the expression of anti-viral genes as well as the effects of adrenergic signaling on the expression of type I interferons (Irwin and Cole, 2011).”
BackgroundSelf-citationβ2-Adrenoreceptor Agonist Inhibits Antigen Cross-Presentation by Dendritic Cells
Hervé, J., Dubreil, L., Tardif, V., Terme, M., Pogu, S., Anegón, I., Rozec, B. R., Gauthier, C., Bach, J., & Blancou, P. (2013) · The Journal of Immunology · doi:10.4049/jimmunol.1201391 · Cited by 94
“Many authors have suggested that stress may regulate immune responses (44).”
BackgroundWhat Are the Health Consequences of Upward Mobility?
Chen, E., Brody, G. H., & Miller, G. E. (2021) · Annual Review of Psychology · doi:10.1146/annurev-psych-033020-122814 · Cited by 108
When grief makes you sick: Bereavement induced systemic inflammation is a question of genotype
Schultze-Florey, C. R., Martínez-Maza, O., Magpantay, L., Breen, E. C., Irwin, M. R., Gündel, H., & O’Connor, M.-F. (2012) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2012.06.009 · Cited by 92
“…caregiving (i.e., those taking care of a severely ill family member) or social isolation is associated with the up-regulated gene expression and production of systemic markers of inflammation (Kiecolt-Glaser et al., 2003; McDade et al., 2006), especially of IL-6, IL-1 and TNF-alpha (Dantzer, 2001).”
BackgroundSelf-citationHigher Vagal Activity as Related to Survival in Patients With Advanced Breast Cancer
Giese‐Davis, J., Wilhelm, F. H., Tamagawa, R., Palesh, O. G., Neri, E., Taylor, C. B., KRAEMER, H. C., & Spiegel, D. (2015) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000167 · Cited by 96
“Several studies demonstrated relationships between sympathetic activity, the immune system (60,81,83), and metastases (84).”
BackgroundO’Sullivan, N. L., & Montgomery, P. C. (2015) · Elsevier eBooks · doi:10.1016/b978-0-12-415847-4.00099-9 · Cited by 93
“Consequently, an extensive, triangular association appears to exist between the endocrine, nervous, and the innate and adaptive immune systems that acts to promote and maintain homeostasis (Befus et al., 1999; Petrovsky, 2001; Webster et al., 2002; Eskandari and Sternberg, 2002; Sternberg, 2006; Irwin and Cole, 2011).”
BackgroundBrain injury instructs bone marrow cellular lineage destination to reduce neuroinflammation
Shi, S. X.-Y., Shi, K., & Liu, Q. (2021) · Science Translational Medicine · doi:10.1126/scitranslmed.abc7029 · Cited by 91
Hostinar, C. E., Nusslock, R., & Miller, G. E. (2018) · Journal of Clinical Child & Adolescent Psychology · doi:10.1080/15374416.2016.1266647 · Cited by 90
“Next, this hypothesis draws further inferences from evidence that peripheral in fl ammation can spread to the brain through multiple mechanisms (Irwin & Cole, 2011).”
Antoni, M. H., Bouchard, L. C., Jacobs, J. M., Lechner, S. C., Jutagir, D. R., Gudenkauf, L. M., Carver, C. S., Lutgendorf, S., Cole, S. W., Lippman, M., et al. (2016) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2016.09.012 · Cited by 89
Self-citationGiletta, M., Slavich, G. M., Rudolph, K. D., Hastings, P. D., Nock, M. K., & Prinstein, M. J. (2018) · Journal of Child Psychology and Psychiatry · doi:10.1111/jcpp.12804 · Cited by 87
“…to the development a number of mental and physical health concerns, including internalizing symptoms (Slavich & Irwin, 2014), sleep disturbances, and fatigue (Irwin & Cole, 2011), all of which have been previously associated with peer victimization (Herge et al., 2016; Reijntjes et al., 2010).”
Knight, J. M., Rizzo, J. D., Logan, B. R., Wang, T., Arevalo, J. M. G., Ma, J., & Cole, S. W. (2015) · Clinical Cancer Research · doi:10.1158/1078-0432.ccr-15-1344 · Cited by 87
“Further, our results are consistent with those from other studies of social adversity that were able to control for smoking (16-19).”
BackgroundMethodResultInfluentialSelf-citationLow Social Support Is Associated With Shorter Leukocyte Telomere Length in Late Life
Carroll, J., Roux, A. V. D., Fitzpatrick, A. L., & Seeman, T. E. (2013) · Psychosomatic Medicine · doi:10.1097/psy.0b013e31828233bf · Cited by 87
Social neuroscience: undoing the schism between neurology and psychiatry
Ibáñez, A. M., García, A. M., Esteves, S., Yoris, A., Muñoz, É., Reynaldo, L., Pietto, M. L., Adolfi, F., & Manes, F. F. (2016) · Social Neuroscience · doi:10.1080/17470919.2016.1245214 · Cited by 86
“Indeed, soluble mediators released by immune cells can affect the central nervous 890 system and alter behavior (Irwin & Cole, 2011; Segerstrom & Miller, 2004).”
BackgroundSnyder‐Mackler, N., Sanz, J., Kohn, J. N., Voyles, T., Piqué-Regi, R., Wilson, M. E., Barreiro, L. B., & Tung, J. (2018) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1811758115 · Cited by 80
“However, recent evidence suggests that social environmental effects in the peripheral immune system also reciprocally influence the brain (78), raising the possibility that effects reported here subsequently feed back to influence social perception and behavior (85).”
BackgroundCole, S. W., Shanahan, M. J., Gaydosh, L. M., & Harris, K. M. (2020) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1821367117 · Cited by 81
“Both gene sets are subject to physiological regulation by tissue injury and microbial stimuli as well as by the neural and endocrine systems (34).”
BackgroundMethodInfluentialSelf-citationMurphy, M. L. M., Slavich, G. M., Rohleder, N., & Miller, G. E. (2013) · Clinical Psychological Science · doi:10.1177/2167702612455743 · Cited by 92
Peripheral inflammation during abnormal mood states in bipolar I disorder
Fiedorowicz, J. G., Prossin, A. R., Johnson, C. P., Christensen, G. E., Magnotta, V. A., & Wemmie, J. A. (2015) · Journal of Affective Disorders · doi:10.1016/j.jad.2015.08.036 · Cited by 81
“Sympathetic nervous system (SNS) related patterns of immune response are designed to steer innate responses away from antiviral and toward natural (non-specific), proinflammatory responses (Irwin and Cole, 2011).”
BackgroundInfluentialIyer, H. S., Hart, J. E., James, P., Elliott, E. G., DeVille, N. V., Holmes, M. D., Vivo, I. D., Mucci, L. A., Laden, F., & Rebbeck, T. R. (2022) · Environment International · doi:10.1016/j.envint.2022.107164 · Cited by 85
“Higher levels of inflammatory markers such as C-reactive protein (CRP), interleukin-6 (IL-6), soluble tumor necrosis factor (sTNFR-2), and lower levels of adipokines may cause cells to adopt several “hallmarks of cancer” (Hanahan and Weinberg, 2011), including increased angiogenesis, cellular proliferation, and escape…”
BackgroundForever Young(er): potential age-defying effects of long-term meditation on gray matter atrophy
Eileen Luders, A., Cherbuin, N., & Kurth, F. (2015) · Frontiers in Psychology · doi:10.3389/fpsyg.2014.01551 · Cited by 79
Sleep characteristics and inflammatory biomarkers among midlife women
Nowakowski, S., Matthews, K. A., von Känel, R., Hall, M. H., & Thurston, R. C. (2018) · SLEEP · doi:10.1093/sleep/zsy049 · Cited by 80
“Higher levels in circulating markers of inflammation, such as interleukin-6 (IL6) and C-reactive protein (CRP), are associated with subsequent CVD events [11, 12], hypertension [13], weight gain [14], type 2 diabetes [15, 16], and depression [17].”
BackgroundThe interpersonally sensitive disposition and health: An integrative review.
Marin, T. J., & Miller, G. E. (2013) · Psychological Bulletin · doi:10.1037/a0030800 · Cited by 79
The effect of cancer treatment on cognitive function.
Asher, A., & Myers, J. S. (2015) · PubMed · Cited by 77
Are Signs of Central Sensitization in Acute Low Back Pain a Precursor to Poor Outcome?
Klyne, D. M., Moseley, G. L., Sterling, M. M., Barbe, M. F., & Hodges, P. W. (2019) · Journal of Pain · doi:10.1016/j.jpain.2019.03.001 · Cited by 80
The Kynurenine Pathway in Traumatic Brain Injury: Implications for Psychiatric Outcomes
Meier, T. B., & Savitz, J. B. (2021) · Biological Psychiatry · doi:10.1016/j.biopsych.2021.05.021 · Cited by 80
Loneliness: An Immunometabolic Syndrome
Pourriyahi, H., Yazdanpanah, N., Saghazadeh, A., & Rezaei, N. (2021) · International Journal of Environmental Research and Public Health · doi:10.3390/ijerph182212162 · Cited by 98
“Further solidifying the pattern of CTRA in loneliness, subjective isolation was found to be correlated with a lower expression of type I interferon (IFN) genes and certain transcripts in the synthesis of immunoglobulin G1 (IgG1), along with the increased expression of pro-inflammatory genes [34,47].”
BackgroundInfluentialCarroll, J., Bower, J. E., & Ganz, P. A. (2021) · Nature Reviews Clinical Oncology · doi:10.1038/s41571-021-00580-3 · Cited by 81
Role of stress in the pathogenesis of cancer (Review)
Lempesis, I. G., Georgakopoulou, V., Papalexis, P., Chrousos, G. P., & Spandidos, D. A. (2023) · International Journal of Oncology · doi:10.3892/ijo.2023.5572 · Cited by 82
Moieni, M., Irwin, M. R., Jevtic, I., Breen, E. C., Cho, H. J., Arevalo, J. M. G., Ma, J., Cole, S. W., & Eisenberger, N. I. (2015) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2015.08.020 · Cited by 81
“ecause of this, it would have been adaptive to temporarily upegulate pro-inflammatory gene expression and down-regulate nti-viral gene expression during periods of perceived social isconnection (Cole, 2013, 2014; Eisenberger and Cole, 2012; rwin and Cole, 2011).”
Self-citationMcGiffin, J. N., Galatzer‐Levy, I. R., & Bonanno, G. A. (2016) · Rehabilitation Psychology · doi:10.1037/rep0000073 · Cited by 82
Wieduwild, É., Girard-Madoux, M. J. H., Quatrini, L., Laprie, C., Chasson, L., Rossignol, R., Bernat, C., Guia, S., & Ugolini, S. (2020) · The Journal of Experimental Medicine · doi:10.1084/jem.20190554 · Cited by 76
Slow Waves Promote Sleep-Dependent Plasticity and Functional Recovery after Stroke
Facchin, L., Schöne, C., Mensen, A., Bandarabadi, M., Pilotto, F., Saxena, S., Libourel, P., Bassetti, C. L., & Adamantidis, A. (2020) · Journal of Neuroscience · doi:10.1523/jneurosci.0373-20.2020 · Cited by 79
“Spontaneous sleep SWs are associated with neuroplastic changes (Tononi and Cirelli, 2006; Puentes-Mestril and Aton, 2017), inflammatory and immunologic adaptative response (Irwin and Cole, 2011), protective functions during infection (Irwin, 2019), and metabolic clearance (Xie et al.”
BackgroundLabus, J. S., Horn, J. D. V., Gupta, A., Alaverdyan, M., Torgerson, C. M., Ashe-McNalley, C., Andrei Irimia, A., Hong, J., Naliboff, B. D., Tillisch, K., et al. (2015) · Pain · doi:10.1097/j.pain.0000000000000196 · Cited by 75
Treadway, M. T., Admon, R., Arulpragasam, A. R., Mehta, M., Douglas, S., Vitaliano, G. D., Olson, D. P., Cooper, J. A., & Pizzagalli, D. A. (2017) · Biological Psychiatry · doi:10.1016/j.biopsych.2017.02.1183 · Cited by 71
Social instability and immunity in rhesus monkeys: the role of the sympathetic nervous system
Capitanio, J. P., & Cole, S. W. (2015) · Philosophical Transactions of the Royal Society B Biological Sciences · doi:10.1098/rstb.2014.0104 · Cited by 76
Self-citationAlloy, L. B., & Nusslock, R. (2019) · Journal of Clinical Child & Adolescent Psychology · doi:10.1080/15374416.2019.1567347 · Cited by 75
“Inflammation is highly adaptive in the short term, accelerating pathogen removal and wound healing (Irwin & Cole, 2011).”
Social ties and health: a social neuroscience perspective
Eisenberger, N. I. (2013) · Current Opinion in Neurobiology · doi:10.1016/j.conb.2013.01.006 · Cited by 82
“Because being disconnected from the social group makes an individual more vulnerable to attack (by predators or hostile con-specifics) and thus increases the likelihood of wounding and infection, the immune system may have evolved to anticipate situations indicative of social disconnection by increasing inflammatory a…”
Wegner, A., Benson, S., Rebernik, L., Spreitzer, I., Jäger, M., Schedlowski, M., Elsenbruch, S., & Engler, H. (2017) · Innate Immunity · doi:10.1177/1753425917707026 · Cited by 74
“Proinflammatory cytokines released by activated immune cells in the periphery signal the brain trough afferent pathways and induce the activation of the hypothalamus–pituitary–adrenal (HPA) axis, ultimately leading the release of cortisol from the adrenal cortex into the circulation.(25) Cortisol, in turn, has potent…”
BackgroundBeach, S. R. H., Lei, M., Brody, G. H., Dogan, M. V., & Philibert, R. A. (2015) · Frontiers in Psychology · doi:10.3389/fpsyg.2015.00676 · Cited by 72
Irwin, M. R., Olmstead, R., Bjurström, M. F., Finan, P. H., & Smith, M. T. (2022) · Pain · doi:10.1097/j.pain.0000000000002811 · Cited by 87
“In turn, sympathetic activation leads to increased release of norepinephrine, binding to b-adrenergic receptors on monocytes,(47) increases in activity of the transcriptional factor, nuclear factor (NF)kB,(5) upregulation of inflammatory transcriptional profiles, and expression of inflammatory mediators.(28,43)”
BackgroundSelf-citationSeeman, T. E., Merkin, S. S., Goldwater, D. S., & Cole, S. W. (2019) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2019.104468 · Cited by 74
Self-citationCo-Morbidities of Interstitial Cystitis
Chelimsky, G. G., Heller, E. A., Buffington, C. A. T., Rackley, R. R., Zhang, D., & Chelimsky, T. C. (2012) · Frontiers in Neuroscience · doi:10.3389/fnins.2012.00114 · Cited by 71
“An abnormal central nervous system drive, with secondary psychoneuro-endocrine-immune dysfunction (Irwin and Cole, 2011) seems likely, as occurs in FM, where heart rate variability analysis demonstrates a skew toward low sympathetic frequencies with reduction or even absence of high parasympathetic frequencies (Staud,…”
BackgroundSocial neuroscience and its potential contribution to psychiatry
Cacioppo, J. T., Cacioppo, S., Dulawa, S. C., & Palmer, A. A. (2014) · World Psychiatry · doi:10.1002/wps.20118 · Cited by 76
“stressor, is associated with the differential expression of pro-inflammatory and antiviral genes (a pattern known as the conserved transcriptional response to adversity) (24-26).”
Cognitive impairment and chemotherapy: a brief overview
Vitali, M., Ripamonti, C. I., Roila, F., Proto, C., Signorelli, D., Imbimbo, M., Corrao, G., Brissa, A., Gallucci, R., de Braud, F., et al. (2017) · Critical Reviews in Oncology/Hematology · doi:10.1016/j.critrevonc.2017.08.001 · Cited by 69
Irwin, M. R., Straub, R. H., & Smith, M. T. (2023) · Nature Reviews Rheumatology · doi:10.1038/s41584-023-00997-3 · Cited by 79
Self-citationWork, meaning, and gene regulation: Findings from a Japanese information technology firm
Kitayama, S., Akutsu, S., Uchida, Y., & Cole, S. W. (2016) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2016.07.004 · Cited by 71
Self-citationdos Santos, R. M. (2020) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2020.100103 · Cited by 74
Cameron, S., Donnelly, A., Broderick, C., Arichi, T., Bartsch, U., Dazzan, P., Elberling, J., Godfrey, E. L., Gringras, P., Heathcote, L. C., et al. (2023) · Allergy · doi:10.1111/all.15818 · Cited by 75
“27 Circadian fluctuations in hormone secretion, including cortisol and subsequent variations in immunological activity, may also increase nocturnal itching, 11,28 for instance due to fluctuating expression of pruritogenic cytokines, such as IL-2 and IL-31.”
BackgroundThe Association Between Loneliness and Inflammation: Findings From an Older Adult Sample
Bogart, K. V., Engeland, C. G., Sliwinski, M. J., Harrington, K., Knight, E. L., Zhaoyang, R., Scott, S., & Graham‐Engeland, J. E. (2022) · Frontiers in Behavioral Neuroscience · doi:10.3389/fnbeh.2021.801746 · Cited by 68
“, 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; Simons et al.”
BackgroundIrwin, M. R. (2022) · Temperature · doi:10.1080/23328940.2022.2109932 · Cited by 80
“Perceived threat also activates physiological responses including activation of the HPA axis, as well as the SNS, which have downstream effects on the immune system leading to increases in markers of inflammation, as well as decreases in antiviral immune responses [30,69,111].”
BackgroundInfluentialSelf-citationRaison, C. L., & Miller, A. H. (2016) · Neuropsychopharmacology · doi:10.1038/npp.2016.194 · Cited by 71
“…conservation-withdrawal (Engel and Schmale, 1972; Eisenberger et al , 2010b; Hannestad et al , 2011) characterized by depressed mood, anhedonia, psychomotor retardation, fatigue, social avoidance, and anorexia (Capuron et al , 2002; Dantzer et al , 2008b; Majer et al , 2008; Irwin and Cole, 2011).”
Beach, S. R. H., Lei, M., Brody, G. H., Kim, S., Barton, A. W., Dogan, M. V., & Philibert, R. A. (2016) · Child Development · doi:10.1111/cdev.12486 · Cited by 67
“…the life history tradition (Belsky, Steinberg, & Draper, 1991; Charnov, 1993) suggests that early adversity may be manifested in changes in the distribution of particular cell types in blood (Irwin & Cole, 2011) as well as in the epigenetic programming of such cells (Miller, Chen, & Parker, 2011).”
BackgroundChronic stress exposure and daily stress appraisals relate to biological aging marker p16INK4a
Rentscher, K. E., Carroll, J., Repetti, R. L., Cole, S. W., Reynolds, B. M., & Robles, T. F. (2018) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2018.12.006 · Cited by 72
“Most well established is the connection between stress and inflammation, as the sympathoadrenal system directly regulates cellular inflammatory signaling, which has been proposed as a key driver of biological aging (Franceschi and Campisi, 2014; Irwin and Cole, 2011; Marsland et al., 2017).”
BackgroundSelf-citation
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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