Stat3 Activation Is Responsible for IL-6-Dependent T Cell Proliferation Through Preventing Apoptosis: Generation and Characterization of T Cell-Specific Stat3-Deficient Mice
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Stat3, a member of STAT, is activated by a variety of cytokines such as IL-6 family of cytokines, granulocyte CSF, epidermal growth factor, and leptin. A recent study with mice genetically deficient in the Stat3 gene has revealed its important role in the early embryogenesis. To assess the function of Stat3 in adult tissues, we disrupted the Stat3 gene specifically in T cells by conditional gene targeting using Cre-loxP system. In Stat3-deficient T cells, IL-6-induced proliferation was severely impaired. IL-6 did not enhance cell cycle progression, but prevented apoptosis of normal T cells. In contrast, IL-6 did not prevent apoptosis of Stat3-deficient T cells. Antiapoptotic protein, Bcl-2, was normally up-regulated in response to IL-6 even in Stat3-deficient T cells. These results demonstrate that Stat3 activation is involved in IL-6-dependent T cell proliferation through prevention of apoptosis independently of Bcl-2.
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T cell-specific STAT3 knockout increases apoptosis and impairs Th17 development.
“Increased apoptosis and impaired Th17 development”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Takeda et al., 1998b
The section ‘IL-6 does not prevent apoptosis of Stat3-deficient T cells’ (page not specified) reports that IL-6 failed to reduce apoptosis in T cell-specific Stat3-deficient cells, supporting the apoptosis portion under that condition. Our copy does not report impaired Th17 development; the Discussion instead reports no apparent abnormality in general T cell development, which does not settle the Th17-specific claim. (LLM, conf=0.89)
Experimental — accuracy not yet measuredSpecific disruption of STAT3 in T cells revealed that STAT3 activation is responsible for IL-6-dependent T cell proliferation through preventing apoptosis.
“Specific disruption of STAT3 in T cells revealed that STAT3 activation is responsible for IL-6-dependent T cell proliferation through preventing apoptosis (13”
From STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration (2002) · cites this paper as [13]
T lymphocyte lineage-specific STAT3-KO mice studies revealed a crucial role of IL-6/STAT3-mediated T cell survival independent of Bcl-2.
“T lymphocyte lineage-specific STAT3-KO mice studies revealed the crucial role of IL-6/STAT3-mediated T cell survival, independent of Bcl-2”
From Targeting Janus Kinases and Signal Transducer and Activator of Transcription 3 To Treat Inflammation, Fibrosis, and Cancer: Rationale, Progress, and Caution (2020) · cites this paper as Takeda et al., 1998
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PI3K integrates the action of insulin and leptin on hypothalamic neurons
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STAT3 signaling controls satellite cell expansion and skeletal muscle repair
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Self-citationIL-6 trans-signaling via STAT3 directs T cell infiltration in acute inflammation
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Involvement of JAK/STAT signaling in the pathogenesis of inflammatory bowel disease
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“T lymphocyte lineage-specific STAT3-KO mice studies revealed the crucial role of IL-6/STAT3-mediated T cell survival, independent of Bcl-2 (Schindler et al., 1992; Takeda et al., 1998).”
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STAT3 Contributes to the Mitogenic Response of Hepatocytes during Liver Regeneration
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Stat3 Activation Links a C/EBPδ to Myostatin Pathway to Stimulate Loss of Muscle Mass
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The astrocyte in multiple sclerosis revisited
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Self-citationThe STAT3 isoforms α and β have unique and specific functions
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STAT3 in Cancer—Friend or Foe?
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- Authors
- Takeda, K., Kaisho, T., Yoshida, N., Takeda, J., Kishimoto, T., & Akira, S.
- Affiliations
- Hyogo Medical University (JP)
- Research Institute, Osaka Maternal and Child Health Center , Izumi, Osaka ,
- The University of Osaka (JP)
- Venue
- The Journal of Immunology
- Publisher
- Oxford University Press (OUP)
- Published
- 1998-11-01
- Volume
- 161
- Issue
- 9
- Pages
- 4652-4660
- ISSN
- 0022-1767 (ISSN-L)
- 1550-6606
- OpenAlex
- W4313347835
- Cited by
- 584
- References
- 52
- Citations by year
- 2026: 3 · 2025: 7 · 2024: 13 · 2023: 11 · 2022: 14 · 2021: 19 · 2020: 19 · 2019: 19 · 2018: 21 · 2017: 20 · 2016: 34 · 2015: 28 · 2014: 27 · 2013: 34 · 2012: 25
- FWCI
- 10.63
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Locations
- The Journal of Immunology (publishedVersion)
- Topics
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Life Sciences › Immunology and Microbiology › Immunology › Psoriasis: Treatment and Pathogenesis
- Keywords
- STAT3, interleukin-6, T cell proliferation, apoptosis, Bcl-2, conditional gene targeting, Cre-loxP system, STAT family, cell cycle progression, anti-apoptotic signaling
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