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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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“Third, our data suggest that ELS-related mechanisms (e.g., Carpenter et al. 2010, 2011; Irwin and Cole 2011; Johnson et al. 2013; Taylor 2010; Tyrka et al. 2013) might provide valuable targets for intervention when developing therapeutic strategies for neuropsychiatric disorders in HIV+ adults with high ELS.”
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“The stress hormone cortisol and catecholamines released from the sympathetic nervous system and adrenal gland have an impact on the expression of NF-jB and I-jB, and a higher NF-jB/I-jB ratio reflects more intense pro-inflammatory processes (Webster et al., 2002; Irwin and Cole, 2011).”
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“Cytokines and chemokines, oxidative stress, and local metabolic changes are produced following microglia activation [8].”
BackgroundInfluentialNeighbourhood-level air pollution and greenspace and inflammation in adults
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“reciprocal to those associated with parasympathetic activity as well as inhibition of innate antiviral responses mediated by the Type I interferon system (Collado-Hidalgo et al., 2006; Irwin and Cole, 2011).”
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“Inflammation has been implicated in brain structural alterations underlying neuropsychiatric disorders via microglia mediated synaptic pruning, neurogenic dysfunction leading to GMV changes (Irwin & Cole, 2011; Valkanova, Ebmeier, & Allan, 2013; Williams et al., 2022).”
Only the Lonely: Expression of Proinflammatory Genes Through Family Cancer Caregiving Experiences
Kim, Y., Cole, S. W., Carver, C. S., Antoni, M. H., & Penedo, F. J. (2020) · Psychosomatic Medicine · doi:10.1097/psy.0000000000000897 · Cited by 17
Self-citationAversa-Marnai, M., Castellano, M., Quartiani, I., Conijeski, D., Perretta, A., Villarino, A., Silva‐Álvarez, V., & Ferreira, A. M. (2021) · Fish & Shellfish Immunology · doi:10.1016/j.fsi.2021.12.029 · Cited by 17
Biological Embedding of Psychosocial Stress Over the Life Course
Eachus, H., & Cunliffe, V. T. (2017) · Elsevier eBooks · doi:10.1016/b978-0-12-811060-7.00012-7 · Cited by 19
Vasileva, L. V., Ivanovska, M. V., Murdjeva, M. A., Saracheva, K. E., & Georgiev, M. I. (2019) · Food and Chemical Toxicology · doi:10.1016/j.fct.2019.03.004 · Cited by 16
“Clarification of the psychological and biological mechanisms by which chronic stress weakens an organism or exacerbates chronic disease would allow the development of behavioral and pharmacological treatment strategies aimed at alleviating or eliminating the harmful effects of stress (Chrousus and Kino, 2007; Jeon and…”
BackgroundTherapeutic Implications of the Microbial Hypothesis of Mental Illness
Savitz, J. B., & Yolken, R. H. (2022) · Current topics in behavioral neurosciences · doi:10.1007/7854_2022_368 · Cited by 15
Bower, J. E., Partridge, A. H., Wolff, A. C., Cole, S. W., Irwin, M. R., Thorner, E. D., Joffe, H., Petersen, L., Crespi, C. M., & Ganz, P. A. (2022) · JNCI Journal of the National Cancer Institute · doi:10.1093/jnci/djac180 · Cited by 18
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“Psychological and emotional stress can alter the sympathetic nervous system and, in turn, the immune system [59].”
BackgroundShao, S., Zou, Y. Z., Kennedy, K. G., Dimick, M. K., MacIntosh, B. J., & Goldstein, B. I. (2023) · The International Journal of Neuropsychopharmacology · doi:10.1093/ijnp/pyad063 · Cited by 17
“…mechanisms focus on the effects of peripheral inflammation on the brain, it is important to also consider the possibility of bidirectional effects, because central inflammation can affect peripheral cytokine levels (Goldstein et al., 2007; Irwin and Cole, 2011; Lampa et al., 2012; Li et al., 2020).”
BackgroundBasarrate, S., Monzel, A. S., Smith, J. L. M., Marsland, A. L., Trumpff, C., & Picard, M. A. (2024) · Psychosomatic Medicine · doi:10.1097/psy.0000000000001275 · Cited by 17
“In turn, the sensitivity of these tissues to neuroendocrine stress mediators may account for the association of life stress with an increased risk of numerous conditions, such as psychiatric disorders, cardiovascular disease, asthma, and immune-related disorders (9 – 12).”
BackgroundThe effect of basketball matches on salivary markers: a systematic review
Kamarauskas, P., & Conte, D. (2021) · Biology of Sport · doi:10.5114/biolsport.2022.107481 · Cited by 16
“Possibly, this outcome was due to the raised level of inflammatory cytokines to elicit greater stimulation of the hypothalamic-pituitary-adrenal axis to release C, which resulted in inhibition of inflammatory cytokine production, responsible for the release of IL-1ß [45].”
BackgroundTraumatic brain injury and neuro-endocrine disruption: Medical and psychosocial rehabilitation
Webb, N. E., Little, B., Loupee-Wilson, S., & Power, E. (2014) · Neurorehabilitation · doi:10.3233/nre-141074 · Cited by 18
“Depression, stressful live events and abnormalities in the immune response are so intertwined that there are 192 articles on the role of stress and abnormal immune responses as a cause of depression (Irwin & Cole, 2011; Mills et al., 2013).”
Use of opioid analgesics or sleeping medication and survival of cancer patients
Chang, W., & Lin, C. (2014) · European Journal of Oncology Nursing · doi:10.1016/j.ejon.2014.11.007 · Cited by 16
Kishan, A. U., Wang, P., Sharif, J., Kupelian, P. A., Steinberg, M. L., & McCloskey, S. A. (2016) · International Journal of Radiation Oncology*Biology*Physics · doi:10.1016/j.ijrobp.2016.01.062 · Cited by 16
Dern, K., Watts, M. R., Werle, B., Eps, A. W. V., Pollitt, C. C., & Belknap, J. K. (2017) · Journal of Veterinary Internal Medicine · doi:10.1111/jvim.14633 · Cited by 16
Flowers, E., Flentje, A., Levine, J. D., Olshen, A. B., Hammer, M. J., Paul, S. M., Conley, Y. P., Miaskowski, C. A., & Kober, K. M. (2019) · Biological Research For Nursing · doi:10.1177/1099800418823286 · Cited by 17
Leckman, J. F., & Vaccarino, F. M. (2014) · Brain Research · doi:10.1016/j.brainres.2014.09.052 · Cited by 15
Vagal nerve activity and cancer prognosis: a systematic review and meta-analysis
Huang, W., Lai, H.-Z., Long, J., Ma, Q., Fu, X., You, F.-M., & Xiao, C. (2025) · BMC Cancer · doi:10.1186/s12885-025-13956-w · Cited by 19
“2) Modulating immunity The VN is an important conduit for bidirectional communication between the brain and the immune system, and may potentially regulate immune suppression to modulate tumor progression [60, 61].”
Bower, J. E., Ganz, P. A., Irwin, M. R., Crespi, C. M., Petersen, L., Asher, A., Hurvitz, S. A., & Cole, S. W. (2024) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2024.02.003 · Cited by 16
“…as mediated by sympathetic nervous system signaling, nor does fatigue track any parallel reduction in inflammatory and Type I IFN activity that would be characteristic of hypothalamus – pituitary – adrenal axis signaling (which represses both of these gene sets in parallel) (Irwin and Cole, 2011).”
Self-citationLiu, X., Zhu, H., Peng, Y., Liu, Y., & Shi, X. (2024) · PLoS ONE · doi:10.1371/journal.pone.0299495 · Cited by 16
“It is likely that practicing Taichi enhances vagal modulation and calms sympathetic activity [48] which provide inhibitory effects on inflammation [49, 50].”
Backgroundda Silva, D. M. A., Lopes, I. S., Oliveira, J. V. S., Júnior, M. A. S., Rebouças, M. D. O., Valentim, J. T., Vale, L. D. C., Capibaribe, V. C. C., de Carvalho, M. A. J., de Aquino, P. É. A., et al. (2024) · Pharmacology Biochemistry and Behavior · doi:10.1016/j.pbb.2024.173778 · Cited by 17
Inflammation and future depressive symptoms among recently bereaved spouses
Wu‐Chung, E. L., LeRoy, A. S., Heijnen, C. J., & Fagundes, C. P. (2021) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2021.105206 · Cited by 18
Psychological Resources and Biomarkers of Health in the Context of Chronic Parenting Stress
Crosswell, A., Sagui-Henson, S. J., Prather, A., Coccia, M. A., Irwin, M. R., & Epel, E. (2021) · International Journal of Behavioral Medicine · doi:10.1007/s12529-021-10007-z · Cited by 16
Self-citationCulture, Mind, and Brain: Emerging Concepts, Models, and Applications
Kirmayer, L. J., Worthman, C. M., Kitayama, S., Lemelson, R., & Cummings, C. A. (2020) · Cited by 15
Rahal, D., Tashjian, S. M., Karan, M., Eisenberger, N. I., Galván, A., Fuligni, A. J., Hastings, P. D., & Cole, S. W. (2023) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2023.106103 · Cited by 18
“Emotion and inflammation are bidirectionally related (Irwin and Cole, 2011).”
BackgroundSelf-citationAdult-Life Occupational Exposures: Enriched Environment or a Stressor for the Aging Brain?
Burzynska, A. Z., Jiao, Y., & Ganster, D. C. (2018) · Work Aging and Retirement · doi:10.1093/workar/way007 · Cited by 15
Ross, K. M., Thomas, J. C., Letourneau, N. L., Campbell, T. S., & Giesbrecht, G. F. (2019) · Biological Psychology · doi:10.1016/j.biopsycho.2019.03.005 · Cited by 15
Addressing Cancer-Related Cognitive Impairment in Cancer Survivorship
Padgett, L. S., Dyk, K. V., Kelly, N. C., Newman, R. M., Hite, S., & Asher, A. (2020) · Oncology Issues · doi:10.1080/10463356.2020.1692601 · Cited by 15
Damage-induced IL-18 stimulates thymic NK cells limiting endogenous tissue regeneration
Granadier, D. W., Cooper, K., Acenas, D. D., II, Kousa, A. I., Warren, M., Hernandez, V. A., Iovino, L., DeRoos, P. C., Lederer, E. E., Shannon-Sevillano, S., et al. (2025) · Nature Immunology · doi:10.1038/s41590-025-02270-z · Cited by 14
“Inflammatory cytokines can stimulate the hypothalamic–pituitary axis, resulting in increased levels of glucocorticoids, which are known to trigger thymus involution 23,25 .”
Nicoloro‐SantaBarbara, J. M., Carroll, J., Minissian, M., Kilpatrick, S. J., Cole, S. W., Merz, C. N. B., & Accortt, E. E. (2022) · American Journal of Reproductive Immunology · doi:10.1111/aji.13619 · Cited by 15
Self-citationLiu, J., Zhang, Y., Li, X., Wang, D., Shi, B., You, Y., Min, L., Luo, B., Li, Y., Di, Q., et al. (2022) · Frontiers in Psychiatry · doi:10.3389/fpsyt.2022.1067890 · Cited by 16
“Peripherally released cytokines send signals via molecular, cellular, and neural routes, ultimately reaching the brain and enhancing central nervous system (CNS) inflammation (18).”
BackgroundMetabolic underpinnings of cancer-related fatigue
Zhang, X., & Perry, R. J. (2024) · American Journal of Physiology-Endocrinology and Metabolism · doi:10.1152/ajpendo.00378.2023 · Cited by 19
Immune dysregulation in bipolar disorder
Argue, B. M., Casten, L. G., McCool, S., Alrfooh, A., Richards, J. G., Wemmie, J. A., Magnotta, V. A., Williams, A. J., Michaelson, J. J., Fiedorowicz, J. G., et al. (2024) · Journal of Affective Disorders · doi:10.1016/j.jad.2025.01.062 · Cited by 14
Zhang, L., Li, T., Chen, L., Wu, F., Xia, W., Huang, M., Guo, Z., Song, L., Yin, H., Zhang, Y., et al. (2021) · EXCLI journal · doi:10.17179/excli2021-3451 · Cited by 15
“…and a marked decrease in SNS activity (Irwin et al., 1999) caused by sleep disturbance, but not acute sleep deprivation, have been revealed to shift the transcriptional profile toward increased inflammatory activity and decreased antiviral responses (Webster et al., 2001; Irwin and Cole, 2011).”
BackgroundRoss, K. M., Cole, S. W., Sanghera, H., Anis, L., Hart, M. J., & Letourneau, N. L. (2021) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2021.100358 · Cited by 15
“is an open access article under t poor health behaviours, such as poor eating habits and less physical activity, and affect activation of stress axes [hypothalamic-pituitary-adrenal (HPA) and sympathetic-adrenal medulla (SAM) axes], which can have downstream effects on the immune system, potentially skewing towards a…”
BackgroundInfluentialSelf-citationThe Central Nervous System and Psychosocial Factors in Primary Microvascular Angina
Cattaneo, M., Hálasz, G., Cattaneo, M. M., Younes, A., Gallino, C., Sudano, I., & Gallino, A. (2022) · Frontiers in Cardiovascular Medicine · doi:10.3389/fcvm.2022.896042 · Cited by 14
“Moreover, sympathetic activation of the adrenal medulla results in the systemic release of catecholamines that multiplies the sympathetic response (30).”
BackgroundBond, D., Andreazza, A., Torres, I., Honer, W., Lam, R. W., & Yatham, L. (2022) · Journal of Affective Disorders · doi:10.1016/j.jad.2022.09.044 · Cited by 11
Evolution, immunity and the emergence of brain superautoantigens
Nataf, S. (2017) · F1000Research · doi:10.12688/f1000research.10950.1 · Cited by 13
Long-Term Associations Between Prenatal Maternal Cortisol and Child Neuroendocrine-Immune Regulation
Riis, J. L., Granger, D. A., Woo, H. W., Voegtline, K., DiPietro, J. A., & Johnson, S. B. (2019) · International Journal of Behavioral Medicine · doi:10.1007/s12529-019-09814-2 · Cited by 14
Maternal subjective social standing is related to inflammation during pregnancy
Scholaske, L., Buß, C., Wadhwa, P. D., & Entringer, S. (2020) · Brain Behavior and Immunity · doi:10.1016/j.bbi.2020.05.023 · Cited by 14
Sleep disorders in cancer: interactions and intrinsic links
Han, C., Li, N., Wang, X., Zhuang, Z., Cao, Q., & Wang, S. (2025) · Frontiers in Oncology · doi:10.3389/fonc.2025.1535442 · Cited by 15
“In fl ammatory response can promote the development, progression, and recurrence of chronic diseases such as cancer and depression (Figure 2) (123).”
Carroll, J., Olmstead, R. E., Cole, S. W., Breen, E. C., Arevalo, J. M. G., & Irwin, M. R. (2023) · GeroScience · doi:10.1007/s11357-023-00741-5 · Cited by 13
“Activation of this system is thought to drive inflammation [67] and elevate mitochondrial metabolism, raising cellular stress and accumulation of damage [30, 31, 64].”
BackgroundSelf-citationGurgoglione, F. L., Rizzello, D., Giacalone, R., Ferretti, M., Vezzani, A., Pfleiderer, B., Pelà, G. M., Panfilis, C. D., Cattabiani, M. A., Benatti, G., et al. (2023) · International Journal of Cardiology · doi:10.1016/j.ijcard.2023.05.027 · Cited by 13
Increased Salivary IL-1 Beta Level Is Associated with Poor Sleep Quality in University Students
Ballestar‐Tarín, M. L., Valle, V. I.-D., Mafla-España, M. A., Cauli, O., & Navarro-Martínez, R. (2023) · Diseases · doi:10.3390/diseases11040136 · Cited by 15
“The latter can induce increases in NF-κ B, inflammatory gene expression, and the production of proinflammatory cytokines, including IL-1 β , thus producing a positive feedback loop with greater increases in IL-1 β levels [41,42].”
BackgroundAssociation of sleep quality and mitochondrial DNA copy number in healthy middle-aged adults
Han, S., Kim, D.-K., Jun, S., & Kim, N. (2023) · Sleep Medicine · doi:10.1016/j.sleep.2023.11.011 · Cited by 15
Ravi, S., Shanahan, M. J., Levitt, B. E., Harris, K. M., & Cole, S. W. (2024) · Scientific Reports · doi:10.1038/s41598-024-51517-6 · Cited by 13
Self-citationBeach, S. R. H., Brody, G. H., Barton, A. W., & Philibert, R. A. (2016) · Development and Psychopathology · doi:10.1017/s0954579416000882 · Cited by 14
“The innate immune system provides immediate defense against infection, and upregulation would be adaptive in response to an environment signaling elevated risk of physical threat (e.g., Irwin & Cole, 2011).”
BackgroundEfficacy of a Stress Management Intervention for Mothers of Children with Cancer
Marsland, A. L., Walsh, C. P., Cleary, J. L., Vaisleib, A. D., Farrell, C. H., Woods, W. C., Tersak, J. M., Wright, A. G. C., & Ewing, L. J. (2020) · Journal of Pediatric Psychology · doi:10.1093/jpepsy/jsaa058 · Cited by 14
Kelechi, T. J., Muise‐Helmericks, R. C., Theeke, L. A., Cole, S. W., Madisetti, M., Mueller, M., & Prentice, M. A. (2021) · BMC Geriatrics · doi:10.1186/s12877-021-02060-w · Cited by 14
“Loneliness has been associated with up-regulated inflammation by enhancing the transcription of genes such as interleukin-1 alpha and beta, interleukin-6, interleukin-8, cyclooxygenase 2, and tumor necrosis factor [39, 40] and the potent pro-inflammatory NF-kappa B gene [41].”
BackgroundSelf-citationPeripheral immune correlates of childhood and adolescent peer relationships: A systematic review
Scott, S., & Manczak, E. M. (2021) · Developmental Psychobiology · doi:10.1002/dev.22119 · Cited by 16
Radmanish, M., Khalfallah, O., Glaichenhaus, N., Forhan, A., Heude, B., Charles, M.-A. A., Davidovic, L., & Plancoulaine, S. (2022) · Brain Behavior & Immunity - Health · doi:10.1016/j.bbih.2022.100429 · Cited by 15
Tang, A., Fox, N. A., Nelson, C. A., Zeanah, C. H., & Slopen, N. B. (2019) · Psychoneuroendocrinology · doi:10.1016/j.psyneuen.2019.104408 · Cited by 13
Gene Expression Profiles in Primary Sjögren's Syndrome With and Without Systemic Manifestations
Vitali, C., Dolcino, M., Papa, N. D., Minniti, A., Pignataro, F. S., Maglione, W., Lunardi, C., & Puccetti, A. (2019) · ACR Open Rheumatology · doi:10.1002/acr2.11082 · Cited by 13
“This is considered the direct consequence of the continuous biological cross talk between the neuroendocrine system and innate immune cell population that induces a reciprocal regulation (34).”
BackgroundCarmeli, C., Kutalik, Z., Mishra, P. P., Porcu, E., Delpierre, C., Delaneau, O., Kelly‐Irving, M., Bochud, M., Dhayat, N. A., Ponte, B., et al. (2021) · Scientific Reports · doi:10.1038/s41598-021-82714-2 · Cited by 13
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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