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• W1910578170 abstract "Abstract Although high mobility group box 1 (HMGB1) in tumor cells is involved in many aspects of tumor progression, its role in tumor immune suppression remains elusive. Host cell-derived IL-10 suppressed a naturally acquired CD8 T cell-dependent antitumor response. The suppressive activity of tumor-associated Foxp3+CD4+CD25+ regulatory T cells (Treg) was IL-10 dependent. Neutralizing HMGB1 impaired tumor cell-promoted IL-10 production by Treg. Short hairpin RNA-mediated knockdown of HMGB1 (HMGB1 KD) in tumor cells did not affect tumor cell growth but uncovered naturally acquired long-lasting tumor-specific IFN-γ– or TNF-α–producing CD8 T cell responses and attenuated their ability to induce Treg, leading to naturally acquired CD8 T cell- or IFN-γ–dependent tumor rejection. The data suggest that tumor cell-derived HMGB1 may suppress naturally acquired CD8 T cell-dependent antitumor immunity via enhancing Treg to produce IL-10, which is necessary for Treg-mediated immune suppression." @default.
• W1910578170 created "2016-06-24" @default.
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• W1910578170 date "2011-07-01" @default.
• W1910578170 modified "2023-10-09" @default.
• W1910578170 title "Knockdown of HMGB1 in Tumor Cells Attenuates Their Ability To Induce Regulatory T Cells and Uncovers Naturally Acquired CD8 T Cell-Dependent Antitumor Immunity" @default.
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• W1910578170 doi "https://doi.org/10.4049/jimmunol.1003378" @default.
• W1910578170 hasPubMedCentralId "https://www.ncbi.nlm.nih.gov/pmc/articles/3119781" @default.
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