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Social-Evaluative Threat and Proinflammatory Cytokine Regulation: An Experimental Laboratory Investigation
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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
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“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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Argaman, Y., Sznycer, D., Crusius, J., van Leeuwen, F., Ohtsubo, Y., Ishihara, H., Zhuang, J.-Y., Zhou, Q.-J., Castelain, T., NETO, F. M. A., et al. (2026) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.2526787123
Nguyen, D., Trinh, C. L. P., Phan, S. V. L., Pham, O., & Nguyen, N. T. T. (2026) · PLoS ONE · doi:10.1371/journal.pone.0357470
최준호, Park, C. I., Kim, S. T., Kang, J. I., Kim, S. J., & Seo, J. H. (2026) · Brain Sciences · doi:10.3390/brainsci16101134
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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Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.
Statistics and arithmetic are recomputed, not judged.
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