The DOI matches its Crossref record, with a small difference in title or year; 36 of the 36 references it cites were found in a registry or an index.
Social-Evaluative Threat and Proinflammatory Cytokine Regulation: An Experimental Laboratory Investigation
Open accessAbstract
This study experimentally tested whether a stressor characterized by social-evaluative threat (SET), a context in which the self can be judged negatively by others, would elicit increases in proinflammatory cytokine activity and alter the regulation of this response. This hypothesis was derived in part from research on immunological responses to social threat in nonhuman animals. Healthy female participants were assigned to perform a speech and a math task in the presence or absence of an evaluative audience (SET or non-SET, respectively). As hypothesized, stimulated production of the proinflammatory cytokine tumor necrosis factor-α (TNF-α) increased from baseline to poststressor in the SET condition, but was unchanged in the non-SET condition. Further, the increases in TNF-α production correlated with participants' cognitive appraisals of being evaluated. Additionally, the ability of glucocorticoids to shut down the inflammatory response was decreased in the SET condition. These findings underscore the importance of social evaluation as a threat capable of eliciting proinflammatory cytokine activity and altering its regulation.
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“In both of these latter studies, however, the effects of acute stress on glucocorticoid resistance were confined to women, highlighting a need for additional research on this topic.”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Dickerson, Gable, Irwin, Aziz, & Kemeny, 2009
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“Evidence that even acute stress can alter glucocorticoid sensitivity is provided by research showing that exposure to social cues indicating an increased risk for possible physical danger induces glucocorticoid resistance.”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Dickerson, Gable, Irwin, Aziz, & Kemeny, 2009
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.
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“Negative social evaluation also elicits autonomic nervous system activation, proinflammatory cytokine increases, and self-reported negative affect (Akinola and Mendes, 2008; Bosch et al., 2009; Dickerson et al., 2009).”
From More than a feeling: A unified view of stress measurement for population science (2018) · cites this paper as Dickerson et al., 2009
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“participants judged these two conditions to be equally challenging, controllable, and difficult”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Dickerson, Gable, et al., 2009
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“individuals who completed the TSST in the presence of socially rejecting raters exhibited greater in vitro LPS-stimulated production of TNFα and greater glucocorticoid resistance than individuals who performed the TSST in the absence of these raters”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Dickerson, Gable, et al., 2009
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“individuals who felt more evaluated in both conditions of the TSST exhibited greater increases in TNFα production, even after controlling for participants' perceptions of TSST-related challenge, controllability, and difficulty”
From From stress to inflammation and major depressive disorder: A social signal transduction theory of depression. (2014) · cites this paper as Dickerson, Gable, et al., 2009
In the citing paper
“Yet, a parallel line of experimental research has demonstrated that different types of stress vary in their salience to the key biological systems thought to mediate stress and negative health outcomes (e.g., Dickerson, Gable, Irwin, Aziz, & Kemeny, 2009; Dickerson & Kemeny, 2004; Kuhlman et al., 2014; Lopez-Duran, Hajal, Olson, Felt, & Vazquez, 2009).”
From Developmental psychoneuroendocrine and psychoneuroimmune pathways from childhood adversity to disease (2017) · cites this paper as Dickerson, Gable, Irwin, Aziz, & Kemeny, 2009
In the citing paper
“Additionally, the perception of threat that leads suicidal individuals to contemplate suicide may activate biological stress responses, including inflammatory responses.[22][23][24]”
From SUICIDAL IDEATION IS ASSOCIATED WITH ELEVATED INFLAMMATION IN PATIENTS WITH MAJOR DEPRESSIVE DISORDER: Research Article: Suicidal Ideation and Inflammation (2013) · cites this paper as [22]
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“In particular, hopelessness and perceived psychological stress may promote inflammation in suicidal individuals.[22,23,37]”
From SUICIDAL IDEATION IS ASSOCIATED WITH ELEVATED INFLAMMATION IN PATIENTS WITH MAJOR DEPRESSIVE DISORDER: Research Article: Suicidal Ideation and Inflammation (2013) · cites this paper as [22]
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Citations
Cites
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From inflammation to sickness and depression: when the immune system subjugates the brain
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Dickerson, S. S., & Kemeny, M. E. (2004) · Psychological Bulletin · doi:10.1037/0033-2909.130.3.355 · Cited by 5,881
Self-citationPsychological stress and the human immune system: a meta-analytic study of 30 Years of inquiry
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The influence of social hierarchy on primate health
Sapolsky, R. M. (2005) · Science · doi:10.1126/science.1106477 · Cited by 2,113 · cited 1×
“Although social threat can elevate glucocorticoids in humans (Dickerson & Kemeny, 2004) and in nonhuman animals (Sapolsky, 2005), certain threats may interfere with the glucocorticoid-driven inhibitory process, thereby leading to simultaneous elevations in glucocorticoid and proinflammatory activity.”
BackgroundAssociations of elevated interleukin-6 and C-reactive protein levels with mortality in the elderly
Harris, T. B., Ferrucci, L., Tracy, R. P., Corti, M. C., Wacholder, S., Ettinger, W. H., Heimovitz, H., Cohen, H. J., & Wallace, R. (1999) · The American Journal of Medicine · doi:10.1016/s0002-9343(99)00066-2 · Cited by 1,488
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A mechanism converting psychosocial stress into mononuclear cell activation
Bierhaus, A., Wolf, J., Andrassy, M., Rohleder, N., Humpert, P. M., Petrov, D., Ferstl, R., von Eynatten, M., Wendt, T., Rudofsky, G., et al. (2003) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.0438019100 · Cited by 927
Cytokines and the Brain: Implications for Clinical Psychiatry
Kronfol, Z., & Remick, D. G. (2000) · American Journal of Psychiatry · doi:10.1176/appi.ajp.157.5.683 · Cited by 784
Research works printed but not linked: 1
- 10.1037/0033-2909.117.3.497 · DOI · Paper page
Cited by
Sorted by citations
Slavich, G. M., & Irwin, M. R. (2014) · Psychological Bulletin · doi:10.1037/a0035302 · Cited by 2,206
Self-citationMore than a feeling: A unified view of stress measurement for population science
Epel, E. S., Crosswell, A. D., Mayer, S. E., Prather, A. A., Slavich, G. M., Puterman, E., & Mendes, W. B. (2018) · Frontiers in Neuroendocrinology · doi:10.1016/j.yfrne.2018.03.001 · Cited by 1,077
“Negative social evaluation also elicits autonomic nervous system activation, proinflammatory cytokine increases, and self-reported negative affect (Akinola and Mendes, 2008; Bosch et al., 2009; Dickerson et al., 2009).”
BackgroundEisenberger, N. I. (2012) · Nature Reviews Neuroscience · doi:10.1038/nrn3231 · Cited by 1,016
Marsland, A. L., Walsh, C., Lockwood, K., & John-Henderson, N. A. (2017) · Brain, Behavior, and Immunity · doi:10.1016/j.bbi.2017.01.011 · Cited by 691
Evolutionary Psychology and the Emotions
Al-Shawaf, L., & Lewis, D. M. G. (2017) · Springer eBooks · doi:10.1007/978-3-319-28099-8_516-1 · Cited by 555
Metadata
- Authors
- Dickerson, S. S., Gable, S. L., Irwin, M. R., Aziz, N., & Kemeny, M. E.
- Affiliations
- University of California, Irvine (US)
- University of California, Santa Barbara (US)
- University of California, Los Angeles (US)
- University of California, San Francisco (US)
- Corresponding author
- Dickerson, Sally S.
- Venue
- Psychological Science
- Publisher
- SAGE Publications
- Published
- 2009-10
- Volume
- 20
- Issue
- 10
- Pages
- 1237-1244
- ISSN
- 0956-7976 (ISSN-L)
- 1467-9280
- PMC
- PMC2761517
- OpenAlex
- W2108820669
- Cited by
- 197
- References
- 36
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 5 · 2023: 10 · 2022: 9 · 2021: 18 · 2020: 11 · 2019: 18 · 2018: 15 · 2017: 14 · 2016: 16 · 2015: 19 · 2014: 15 · 2013: 9 · 2012: 17
- FWCI
- 3.32
- Type
- journal article
- Language
- en
- Open access
- green
- www.ncbi.nlm.nih.gov
- Locations
- Psychological Science (publishedVersion)
- PubMed (publishedVersion)
- PubMed Central (acceptedVersion)
- Funders
- National Center for Research Resources ((M01 RR00865), M01RR000865)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
- Keywords
- social-evaluative threat, inflammatory cytokines, TNF-α, stress, cognitive appraisal, glucocorticoids, inflammation modulation, social evaluation, speaking tasks, audience evaluation
- MeSH terms
- Adult, Analysis of Variance, Blood Pressure, Emotions, Female, Glucocorticoids, Humans, Mathematics, Surveys and Questionnaires, Self Concept, Social Behavior, Speech, Stress, Psychological, Task Performance and Analysis, Tumor Necrosis Factor-alpha, Cytokines, Young Adult
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