The DOI matches its Crossref record; 95 of the 97 references it cites were found in a registry or an index.
Stress and immunity: An integrated view of relationships between the brain and the immune system
Abstract
The old notion that stress exacerbates the progression of physical illness via its corticosteroid-mediated immunosuppressive effects must be revised. Experimental and clinical studies demonstrate that both laboratory and natural stressors alter the activities of lymphocytes and macrophages in a complex way that depends on the type of immune response, the physical and psychological characteristics of the stressor and the timing of stress relative to the induction and expression of the immune event. The influences of stress on immunity are mediated not only by glucocorticoids but also by catecholamines, endogenous opioids and pituitary hormones such as growth hormone. Sensitivity of the immune system to stress is not simply fortuitous but is an indirect consequence of the regulatory reciprocal influences that exist between the immune system and the central nervous system. The immune system receives signals from the brain and the neuroendocrine system via the autonomic nervous system and hormones and sends information to the brain via cytokines. These connections appear to be part of a long-loop regulatory feedback system that plays an important role in the coordination of behavioral and physiological responses to infection and inflammation.
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“However, these peripherally produced cytokines also act on the brain to cause the aforementioned behavioural symptoms of sickness.”
From From inflammation to sickness and depression: when the immune system subjugates the brain (2008) · cites this paper as [3]
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Metadata
- Authors
- Dantzer, R., & Kelley, K. W.
- Affiliations
- Inserm (FR)
- University of Illinois Urbana-Champaign (US)
- Venue
- Life Sciences
- Publisher
- Elsevier BV
- Published
- 1989
- Volume
- 44
- Issue
- 26
- Pages
- 1995-2008
- ISSN
- 0024-3205 (ISSN-L)
- OpenAlex
- W2012740861
- Cited by
- 534
- References
- 97
- Citations by year
- 2025: 2 · 2024: 8 · 2023: 10 · 2022: 7 · 2021: 16 · 2020: 9 · 2019: 11 · 2018: 9 · 2017: 7 · 2016: 8 · 2015: 18 · 2014: 9 · 2013: 15 · 2012: 16
- FWCI
- 6.21
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Life Sciences (publishedVersion)
- PubMed (publishedVersion)
- HAL (submittedVersion)
- Funders
- National Institutes of Health (AG 06246)
- U.S. Department of Agriculture (86-CRCR-I-2003)
- Topics
- Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › Cancer, Stress, Anesthesia, and Immune Response
- Life Sciences › Neuroscience › Biological Psychiatry › Tryptophan and brain disorders
- Keywords
- stress, immunity, neuroimmune interactions, glucocorticoids, immunosuppression, catecholamines, endogenous opioids, growth hormone, cytokines, autonomic nervous system, neuroendocrine regulation, lymphocytes, macrophages, infection, inflammation
- MeSH terms
- Animals, Biological Factors, Brain, Hormones, Humans, Immune Tolerance, Stress, Physiological, Stress, Psychological, Cytokines, Neurotransmitter Agents
About these checks
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.
Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.
What counts as a claim ›How we measure confidence ›How we check this ›
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