Constitutively activated Jak-STAT pathway in T cells transformed with HTLV-I
Abstract
Human T cell lymphotropic virus I (HTLV-I) is the etiological agent for adult T cell leukemia and tropical spastic paraparesis (also termed HTLV-I-associated myelopathy). HTLV-I-infected peripheral blood T cells exhibit an initial phase of interleukin-2 (IL-2)-dependent growth; over time, by an unknown mechanism, the cells become IL-2-independent. Whereas the Jak kinases Jak1 and Jak3 and the signal transducer and activator of transcription proteins Stat3 and Stat5 are activated in normal T cells in response to IL-2, this signaling pathway was constitutively activated in HTLV-I-transformed cells. In HTLV-I-infected cord blood lymphocytes, the transition from IL-2-dependent to IL-2-independent growth correlated with the acquisition of a constitutively activated Jak-STAT pathway, which suggests that this pathway participates in HTLV-I-mediated T cell transformation.
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Either or both STAT3 and NF-κB are activated in cells transformed with HTLV-1, v-src, abl, bcr-abl or v-eyk.
“Additionally, either or both are activated in cells transformed with HTLV-1 (311), v-src (312), abl (313), bcr-abl or v-eyk (314).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [311]
HTLV-I, Epstein-Barr virus and papilloma virus activate STAT3 and NF-κB.
“Both hepatitis B and hepatitis C viruses, which induce hepatitis and cause hepatocellular carcinoma, activate STAT3 (328–330), while HTLV-I, Epstein–Barr virus and papilloma virus activate STAT3 and NF-κB (311, 331, 332).”
From IL-6 in inflammation, autoimmunity and cancer (2021) · cites this paper as [311]
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- Authors
- Migone, T.-S., Lin, J.-X., Cereseto, A., Mulloy, J. C., O'Shea, J. J., Franchini, G., & Leonard, W. J.
- Affiliations
- National Institutes of Health (US)
- Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, MD 20892, USA.
- Venue
- Science
- Published
- 1995-07-07
- Volume
- 269
- Issue
- 5220
- Pages
- 79-81
- ISSN
- 0036-8075 (ISSN-L)
- 1095-9203
- OpenAlex
- W2097765112
- Cited by
- 557
- References
- 0
- Citations by year
- 2026: 4 · 2025: 3 · 2024: 7 · 2023: 4 · 2022: 7 · 2021: 9 · 2020: 12 · 2019: 7 · 2018: 8 · 2017: 4 · 2016: 6 · 2015: 13 · 2014: 12 · 2013: 16 · 2012: 13
- FWCI
- 18.63
- Type
- journal article
- Language
- en
- Open access
- closed
- Locations
- Science (publishedVersion)
- PubMed (publishedVersion)
- Institutional Research Information System (Università degli Studi di Trento) (submittedVersion)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and Retrovirus Studies
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Biochemistry, Genetics and Molecular Biology › Cancer Research › NF-κB Signaling Pathways
- Keywords
- HTLV-1, JAK/STAT signaling, T-cell transformation, adult T-cell leukemia/lymphoma, tropical spastic paraparesis, IL-2 independence, JAK1, JAK3, STAT3, STAT5, cord blood lymphocytes, viral oncogenesis
- MeSH terms
- Base Sequence, Cell Line, Transformed, Cell Transformation, Viral, Cells, Cultured, DNA-Binding Proteins, Enzyme Activation, Fetal Blood, Humans, Interleukin-2, Milk Proteins, Molecular Sequence Data, Phosphorylation, Protein-Tyrosine Kinases, T-Lymphocytes, Human T-lymphotropic virus 1, Receptors, Interleukin-2, Signal Transduction, Trans-Activators, STAT3 Transcription Factor, STAT5 Transcription Factor, Janus Kinase 1, Janus Kinase 3
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