ArticlePloS one2013
Induction of regulatory T cells by high-dose gp96 suppresses murine liver immune hyperactivation.
Article in PloS one, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
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Who cites it
11 citing papers in PubMed, 21 citations in OpenAlex.
- miR-223-3p predicts prognosis of hepatitis B virus-related acute-on-chronic liver failure and is involved in hepatocyte injury via HSP90B1.Hereditas · 2025Article
- HSP90 multi-functionality in cancer.Frontiers in immunology · 2024Review
- Review
- Mechanisms of drug resistance to immune checkpoint inhibitors in non-small cell lung cancer.Frontiers in immunology · 2023Review
- Induction of Foxp3 and activation of Tregs by HSP gp96 for treatment of autoimmune diseases.iScience · 2021Article
- The HSP Immune Network in Cancer.Frontiers in immunology · 2021Review
- Immunosurveillance of cancer and the heat shock protein-CD91 pathway.Cellular immunology · 2019Article
- HSPs drive dichotomous T-cell immune responses via DNA methylome remodelling in antigen presenting cells.Nature communications · 2017Article
- Article
- Glucose-regulated proteins in cancer: molecular mechanisms and therapeutic potential.Nature reviews. Cancer · 2014Review
- Hepatic expression of metallothionein I/II, glycoprotein 96, IL-6, and TGF- β in rat strains with different susceptibilities to experimental autoimmune encephalomyelitis.Clinical & developmental immunology · 2013Article
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Authors and funding
10 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Immunization with high-dose heat shock protein gp96, an endoplasmic reticulum counterpart of the Hsp90 family, significantly enhances regulatory T cell (Treg) frequency and suppressive function. Here, we examined the potential role and mechanism of gp96 in regulating immune-mediated hepatic injury in mice. High-dose gp96 immunization elicited rapid and long-lasting protection of mice against concanavalin A (Con A)-and anti-CD137-induced liver injury, as evidenced by decreased alanine aminotransaminase (ALT) levels, hepatic necrosis, serum pro-inflammatory cytokines (IFN-γ, TNF-α, and IL-6), and number of IFN-γ (+) CD4(+) and IFN-γ (+) CD8(+) T cells in the spleen and liver. In contrast, CD4(+)CD25(+)Foxp3(+) Treg frequency and suppressive function were both increased, and the protective effect of gp96 could be generated by adoptive transfer of Treg cells from gp96-immunized mice. In vitro co-culture experiments demonstrated that gp96 stimulation enhanced Treg proliferation and suppressive function, and up-regulation of Foxp3, IL-10, and TGF-β1 induced by gp96 was dependent on TLR2- and TLR4-mediated NF-κB activation. Our work shows that activation of Tregs by high-dose gp96 immunization protects against Con A- and anti-CD137-induced T cell-hepatitis and provides therapeutic potential for the development of a gp96-based anti-immune hyperactivation vaccine against immune-mediated liver destruction.
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