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Cited by 983Stress Responses and CortisolAdrenal Hormones and DisordersCytokine Signaling Pathways and Interactions

The DOI matches its Crossref record; 76 of the 77 references it cites were found in a registry or an index.

Stress Hormones, Proinflammatory and Antiinflammatory Cytokines, and Autoimmunity

ELENKOV, ILIA J., CHROUSOS, GEORGE P.·2002·Annals of the New York Academy of Sciences
DOI 10.1111/j.1749-6632.2002.tb04229.x
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Abstract

A bstract : Recent evidence indicates that glucocorticoids and catecholamines, the major stress hormones, inhibit the production of proinflammatory cytokines, such as interleukin (IL)‐12, tumor necrosis factor (TNF)‐α, and interferon (IFN)‐γ, whereas they stimulate the production of antiinflammatory cytokines, such as IL‐10, IL‐4, and transforming growth factor (TGF)‐β. Thus, systemically, an excessive immune response, through activation of the stress system, stimulates an important negative feedback mechanism, which protects the organism from an “overshoot” of proinflammatory cytokines and other products of activated macrophages with tissue‐damaging potential. Conversely, in certain local responses and under certain conditions, stress hormones actually may boost regional immune responses, through induction of TNF‐α, IL‐1, and IL‐8, and by inhibiting TGF‐β production. Therefore, conditions that are associated with significant changes in stress system activity, such as acute or chronic stress, cessation of chronic stress, severe exercise, and pregnancy and the postpartum period, through modulation of the systemic or local pro/antiinflammatory cytokine balance, may suppress or potentiate autoimmune diseases activity and/or progression.

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  1. 10.1210/jc.81.10.3604 · DOI

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Metadata

Authors
ELENKOV, I. J., & CHROUSOS, G. P.
Affiliations
National Institutes of Health (US)
Corresponding author
ELENKOV, ILIA J.
ORCID
CHROUSOS, GEORGE P.
Venue
Annals of the New York Academy of Sciences
Publisher
Wiley
Published
2002-06
Volume
966
Issue
1
Pages
290-303
ISSN
  • 0077-8923 (ISSN-L)
  • 1749-6632
DOI
10.1111/j.1749-6632.2002.tb04229.x
OpenAlex
W1987912134
Cited by
983
References
77
Citations by year
2026: 18 · 2025: 18 · 2024: 32 · 2023: 29 · 2022: 32 · 2021: 39 · 2020: 35 · 2019: 52 · 2018: 33 · 2017: 34 · 2016: 42 · 2015: 51 · 2014: 43 · 2013: 46 · 2012: 52
FWCI
4.21
Type
journal article
Language
en
Open access
closed
Licence
onlinelibrary.wiley.com/termsAndConditions#vor (vor, 1333 d)
Locations
  • Annals of the New York Academy of Sciences (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Neuroscience › Behavioral Neuroscience › Stress Responses and Cortisol
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
Keywords
stress hormones, glucocorticoids, catecholamines, inflammatory cytokines, autoimmunity, autoimmune disease, IL-12, TNF-α, interferon-gamma, IL-10, TGF-beta, negative feedback regulation, chronic stress, physical activity, pregnancy, postpartum period
MeSH terms
Animals, Autoimmune Diseases, Catecholamines, Feedback, Female, Gene Expression Regulation, Glucocorticoids, Humans, Hypothalamo-Hypophyseal System, Macrophage Activation, Male, Pregnancy, Pregnancy Complications, Puerperal Disorders, Rats, Inbred Lew, Stress, Physiological, Sympathetic Nervous System, Neuroimmunomodulation, Autoimmunity, Cytokines, Antigen Presentation, Th1 Cells, Th2 Cells, Models, Immunological, Inflammation Mediators, Rats

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