期刊
JOURNAL OF IMMUNOLOGY
卷 187, 期 1, 页码 118-125出版社
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.1003378
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资金
- National Institutes of Health [R01CA108813, R01CA108813-04S2, R01AI076060, CA106662, P01CA73743]
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-gamma- or TNF-alpha-producing CD8 T cell responses and attenuated their ability to induce Treg, leading to naturally acquired CD8 T cell- or IFN-gamma-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. The Journal of Immunology, 2011, 187: 118-125.
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