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Cited by 42T-cell and B-cell ImmunologyPsoriasis: Treatment and PathogenesisImmunotoxicology and immune responses

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In vitro generation of IL-10-producing regulatory CD4+ T cells is induced by immunosuppressive drugs and inhibited by Th1- and Th2-inducing cytokines

O'Garra, Anne, Barrat, Franck J·2003·Immunology Letters
DOI 10.1016/s0165-2478(02)00239-0
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  • Signaling through NR3C1 varies depending on T cell phenotype; in effector T cells, DEXA inhibits pro-inflammatory cytokine production and proliferation.

    “Signaling through NR3C1 varies depending on T cell phenotype: for example, in effector T cells, DEXA inhibits pro-inflammatory cytokine production and proliferation, potentially reducing harmful inflammation [O’Garra & Barrat, 2003].”

    From Cell signaling pathways discovery from multi-modal data (2025) · cites this paper as O’Garra & Barrat, 2003

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Research works printed but not linked: 39

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Metadata

Authors
O'Garra, A., & Barrat, F. J.
Affiliations
Dynavax Technologies (United States) (US)
ORCID
Barrat, Franck J
Venue
Immunology Letters
Publisher
Elsevier BV
Published
2003-01
Volume
85
Issue
2
Pages
135-139
ISSN
0165-2478 (ISSN-L)
DOI
10.1016/s0165-2478(02)00239-0
OpenAlex
W2065427225
Cited by
42
References
1
Citations by year
2025: 1 · 2022: 1 · 2021: 1 · 2018: 2 · 2014: 2 · 2012: 2
FWCI
0.44
Type
journal article
Language
en
Open access
closed
Licence
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
Locations
  • Immunology Letters (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
  • Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
  • Life Sciences › Immunology and Microbiology › Immunology › Immunotoxicology and immune responses
Keywords
regulatory T cells, IL-10, CD4+ T cells, immunosuppressants, Th1 cytokines, Th2 cytokines, Treg differentiation
MeSH terms
Animals, Cell Differentiation, Cholecalciferol, Dexamethasone, Humans, Immunosuppressive Agents, Signal Transduction, CD4-Positive T-Lymphocytes, Cytokines, Interleukin-10, Th1 Cells, Th2 Cells

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