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Cited by 277T-cell and B-cell ImmunologyAdrenal Hormones and DisordersEstrogen and related hormone effects

The DOI matches its Crossref record; 21 of the 21 references it cites were found in a registry or an index.

Dehydroepiandrosterone enhances IL2 production and cytotoxic effector function of human T cells.

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Suzuki, Tomoko, Suzuki, Noboru, Daynes, Raymond A., Engleman, Edgar G.·1991·Clinical Immunology and Immunopathology
DOI 10.1016/s0090-1229(05)80024-8
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Abstract

Dehydroepiandrosterone (DHEA) is the most abundant adrenal steroid hormone in humans. Although it is well established that DHEA serves as an intermediate in sex steroid synthesis, recent studies in mice suggest that DHEA may also be a physiologic regulator of IL2 secretion. To explore the effect of DHEA on the human immune system, T lymphocytes from healthy adults were exposed to DHEA followed by stimulation with mitogens or antigen. Upon activation with a variety of stimuli, T cells pretreated with 10(-8) to 10(-11) M DHEA produced significantly greater amounts of IL2 and mediated more potent cytotoxicity than T cells activated in the absence of this steroid hormone. The peak effect of DHEA was observed at 10(-9) M, the concentration of hormone present in the blood of normal adults. In contrast to its effect on murine T cells, the IL2 enhancing effect of DHEA on human lymphocytes was limited to fresh CD4+ T cells and CD4+ clones; neither fresh CD8+ cells nor CD8+ clones were directly affected by DHEA treatment, although CD8+ cells stimulated in the presence of CD4+ cells and DHEA demonstrated enhanced cytotoxicity. The enhancing effect of DHEA was also detected at the level of IL2 mRNA, suggesting that DHEA may act as a transcriptional enhancer of the IL2 gene in CD4+ T cells. These results corroborate and extend earlier studies in mice and suggest a physiologic role for DHEA in regulating the human immune response.

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Crossref · 10.1016/s0090-1229(05)80024-8

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Metadata

Authors
Suzuki, T., Suzuki, N., Daynes, R. A., & Engleman, E. G.
Affiliations
  • Stanford Medicine (US)
  • University of Utah (US)
Corresponding author
Engleman, Edgar G.
ORCID
Venue
Clinical Immunology and Immunopathology
Publisher
Elsevier BV
Published
1991-11
Volume
61
Issue
2
Pages
202-211
ISSN
0090-1229 (ISSN-L)
DOI
10.1016/s0090-1229(05)80024-8
OpenAlex
W1980941499
Cited by
277
References
21
Citations by year
2026: 2 · 2025: 3 · 2024: 3 · 2023: 2 · 2022: 6 · 2021: 3 · 2020: 5 · 2019: 4 · 2018: 9 · 2017: 5 · 2016: 4 · 2015: 6 · 2014: 7 · 2013: 1 · 2012: 4
FWCI
2.79
Type
journal article
Language
en
Open access
Licence
Locations
  • Clinical Immunology and Immunopathology (publishedVersion, cc-by-nc-nd)
  • PubMed (publishedVersion)
Funders
  • National Institutes of Health (5u01ai025922-05)
  • National Cancer Institute (CA-24607)
  • National Institute of Allergy and Infectious Diseases (AI25922)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Health Sciences › Medicine › Endocrinology, Diabetes and Metabolism › Adrenal Hormones and Disorders
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Endocrinology › Estrogen and related hormone effects
Keywords
dehydroepiandrosterone, interleukin-2, T cell activation, cytotoxic T lymphocytes, CD4+ T cells, CD8+ T cells, steroid hormones, T cell cytotoxicity
MeSH terms
Cells, Cultured, Dehydroepiandrosterone, Humans, Interleukin-2, RNA, Messenger, T-Lymphocytes, Cytotoxic, CD4 Antigens, Interleukin-4, CD8 Antigens

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