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Cited by 278Cytokine Signaling Pathways and Interactionsinterferon and immune responsesT-cell and B-cell Immunology

The DOI matches its Crossref record; 57 of the 57 references it cites were found in a registry or an index.

Interferon- Activates Multiple STAT Proteins and Upregulates Proliferation-Associated IL-2R, c-myc, and pim-1 Genes in Human T Cells

Matikainen, Sampsa, Sareneva, Timo, Ronni, Tapani, Lehtonen, Anne, Koskinen, Päivi J., Julkunen, Ilkka·1999·Blood
DOI 10.1182/blood.v93.6.1980.406k20_1980_1991
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Abstract

Interferon- (IFN-) is a pleiotropic cytokine that has antiviral, antiproliferative, and immunoregulatory functions. There is increasing evidence that IFN- has an important role in T-cell biology. We have analyzed the expression ofIL-2R, c-myc, and pim-1 genes in anti-CD3–activated human T lymphocytes. The induction of these genes is associated with interleukin-2 (IL-2)–induced T-cell proliferation. Treatment of T lymphocytes with IFN-, IL-2, IL-12, and IL-15 upregulated IL-2R, c-myc, andpim-1 gene expression. IFN- also sensitized T cells to IL-2–induced proliferation, further suggesting that IFN- may be involved in the regulation of T-cell mitogenesis. When we analyzed the nature of STAT proteins capable of binding to IL-2R,pim-1, and IRF-1 GAS elements after cytokine stimulation, we observed IFN-–induced binding of STAT1, STAT3, and STAT4, but not STAT5 to all of these elements. Yet, IFN- was able to activate binding of STAT5 to the high-affinity IFP53 GAS site. IFN- enhanced tyrosine phosphorylation of STAT1, STAT3, STAT4, STAT5a, and STAT5b. IL-12 induced STAT4 and IL-2 and IL-15 induced STAT5 binding to the GAS elements. Taken together, our results suggest that IFN-, IL-2, IL-12, and IL-15 have overlapping activities on human T cells. These findings thus emphasize the importance of IFN- as a T-cell regulatory cytokine.

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Crossref · 10.1182/blood.v93.6.1980.406k20_1980_1991

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Research works printed but not linked: 1

  1. Herbermann, 1997, Effect of α-interferons on immune function., Semin Oncol, 24, S9

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Metadata

Authors
Matikainen, S., Sareneva, T., Ronni, T., Lehtonen, A., Koskinen, P. J., & Julkunen, I.
Affiliations
  • Åbo Akademi University (FI)
  • From the Department of Virology, National Public Health Institute, Helsinki, Finland; and Turku Centre for Biotechnology, University of Turku and Åbo Akademi University, Turku, Finland.
ORCID
Venue
Blood
Publisher
American Society of Hematology
Published
1999-03-15
Volume
93
Issue
6
Pages
1980-1991
ISSN
  • 0006-4971 (ISSN-L)
  • 1528-0020
DOI
10.1182/blood.v93.6.1980.406k20_1980_1991
OpenAlex
W1551136390
Cited by
278
References
57
Citations by year
2026: 6 · 2025: 5 · 2024: 7 · 2023: 4 · 2022: 4 · 2021: 9 · 2020: 2 · 2019: 4 · 2018: 7 · 2017: 13 · 2016: 9 · 2015: 10 · 2014: 11 · 2013: 15 · 2012: 16
FWCI
5.92
Type
journal article
Language
en
Open access
closed
Locations
  • Blood (publishedVersion)
  • PubMed (publishedVersion)
Topics
  • Life Sciences › Immunology and Microbiology › Immunology › Cytokine Signaling Pathways and Interactions
  • Life Sciences › Immunology and Microbiology › Immunology › interferon and immune responses
  • Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
Keywords
interferon-alpha, STAT proteins, T cell proliferation, IL-2 receptor alpha, c-Myc, PIM-1, STAT1, STAT3, STAT4, STAT5, gene expression regulation, tyrosine phosphorylation, IL-12, IL-15, interleukin-2, interferon-stimulated genes, T cell regulation
MeSH terms
DNA, DNA-Binding Proteins, Gene Expression Regulation, Humans, Lymphocyte Activation, Milk Proteins, Proto-Oncogene Proteins, Recombinant Proteins, RNA, Messenger, T-Lymphocytes, Receptors, Interleukin-2, Trans-Activators, Genes, myc, Interferon-alpha, CD3 Complex, Protein Serine-Threonine Kinases, Interleukin-12, Phosphotyrosine, Interleukin-15, Tumor Suppressor Proteins, STAT1 Transcription Factor, STAT3 Transcription Factor, STAT4 Transcription Factor, STAT5 Transcription Factor, Proto-Oncogene Proteins c-pim-1

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