A Critical Role for Stat3 Signaling in Immune Tolerance
Open accessAbstract
Antigen-presenting cells (APCs) can induce T cell activation as well as T cell tolerance. The molecular mechanisms by which APCs regulate this critical decision of the immune system are not well understood. Here we show that Stat3 signaling plays a critical role in the induction of antigen-specific T cell tolerance. Targeted disruption of Stat3 signaling in APCs resulted in priming of antigen-specific CD4(+) T cells in response to an otherwise tolerogenic stimulus in vivo. Furthermore, APCs devoid of Stat3 effectively break antigen-specific T cell anergy in vitro. Conversely, increased Stat3 activity in APCs led to impaired antigen-specific T cell responses. Stat3 signaling provides, therefore, a novel molecular target for manipulation of immune activation/tolerance, a central decision with profound implications in autoimmunity, transplantation, and cancer immunotherapy.
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IL-6- and IL-10-stimulated STAT3 suppresses dendritic cell maturation and activation and promotes immune tolerance.
“IL-6– and IL-10–stimulated STAT3 is also known to suppress DC maturation and activation and promote immune tolerance”
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 Cheng et al., 2003
Anti-hemagglutinin CD4+ transgenic T cells are rendered tolerant after in vivo exposure to high doses of hemagglutinin peptide.
“Studies with a T cell receptor–transgenic model have demonstrated that anti-hemagglutinin CD4+ transgenic T cells are rendered tolerant after in vivo exposure to high doses of hemagglutinin peptide29.”
From The histone deacetylase HDAC11 regulates the expression of interleukin 10 and immune tolerance (2009) · cites this paper as [29]
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References 35 · Cited by 377
- Authors
- Cheng, F., Wang, H.-W., Cuenca, A., Huang, M., Ghansah, T., Brayer, J., Kerr, W. G., Takeda, K., Akira, S., Schoenberger, S. P., Yu, H., Jove, R., & Sotomayor, E. M.
- Affiliations
- University of South Florida (US)
- The University of Osaka (JP)
- La Jolla Institute for Immunology (US)
- Corresponding author
- Sotomayor, Eduardo M.
- ORCID
- Venue
- Immunity
- Publisher
- Elsevier BV
- Published
- 2003-09
- Volume
- 19
- Issue
- 3
- Pages
- 425-436
- ISSN
- 1074-7613 (ISSN-L)
- OpenAlex
- W2008267385
- Cited by
- 377
- References
- 35
- Citations by year
- 2026: 3 · 2025: 3 · 2024: 10 · 2023: 10 · 2022: 9 · 2021: 16 · 2020: 13 · 2019: 12 · 2018: 16 · 2017: 24 · 2016: 12 · 2015: 8 · 2014: 19 · 2013: 26 · 2012: 20
- FWCI
- 7.03
- Type
- journal article
- Language
- en
- Open access
- bronze
- doi.org
- Licence
- Locations
- Immunity (publishedVersion)
- PubMed (publishedVersion)
- Funders
- National Institutes of Health (5k08ca078656-03)
- National Cancer Institute (R01CA087583, CA78656, R01CA100850, CA87583, CA100850)
- Topics
- Life Sciences › Immunology and Microbiology › Immunology › T-cell and B-cell Immunology
- Health Sciences › Medicine › Oncology › Cytokine Signaling Pathways and Interactions
- Life Sciences › Immunology and Microbiology › Immunology › Immunotherapy and Immune Responses
- Keywords
- STAT3 signaling, immune tolerance, antigen-presenting cells, T cell anergy, CD4+ T cells, T cell activation, autoimmunity, transplantation, cancer immunotherapy
- MeSH terms
- Animals, Antigen-Presenting Cells, DNA-Binding Proteins, Enzyme Inhibitors, Immune Tolerance, Macrophages, Signal Transduction, CD4-Positive T-Lymphocytes, Trans-Activators, Tyrphostins, STAT3 Transcription Factor, Mice
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