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- W2031188093 abstract "To investigate the effect of high-mobility group box 1 (HMGB1) protein on the regulatory T cells (Tregs) in vitro and its potential regulating mechanism in mice. Splenic CD4+CD25+ Tregs and CD4+CD25− T cells were isolated. The time-dependent and dose-dependent responses between HMGB1 stimulation and cytotoxic T lymphocyte–associated antigen 4 (CTLA-4) and forkhead/winged helix transcription factor p3 (Foxp3) expressions were analyzed. The secretion of various cytokines in the cell suspensions and the proliferation of CD4+CD25− T cells were determined. HMGB1 was found to be able to markedly down-regulate the expressions of CTLA-4 and Foxp3, especially at 72 h group and in 1,000 ng/mL group (both P < 0.01). The expression of Foxp3 mRNA showed a similar tendency as Foxp3 protein (P < 0.05 or P < 0.01). The secretion of interleukin (IL)-10 from Tregs was decreased when the concentration of HMGB1 was increased. The suppressive activity of proliferation of CD4+CD25− T cells exceeded 90% when the ratio of Tregs to CD4+CD25− T cells was 1:1; meanwhile, the proliferation of CD4+CD25− T cells was enhanced when cultured with HMGB1-stimulated Tregs. In the culture of HMGB1-stimulated Tregs, IL-2 and interferon-γ levels were elevated; whereas IL-4 and IL-10 decreased in CD4+CD25− T cells after the increased concentration of HMGB1 in comparison with unstimulated-Treg group. HMGB1 stimulation can result in markedly down-regulatory expressions of CTLA-4 as well as in Foxp3 expression and secretion of IL-10 from splenic Tregs in mice. HMGB1 appears to be involved in modulating cell-mediated immunity by influencing proliferation of effector T cells, secretion of IL-2, and cell polarization." @default.
- W2031188093 created "2016-06-24" @default.
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- W2031188093 date "2011-02-01" @default.
- W2031188093 modified "2023-10-07" @default.
- W2031188093 title "The Potential Effect and Mechanism of High-Mobility Group Box 1 Protein on Regulatory T Cell-Mediated Immunosuppression" @default.
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- W2031188093 doi "https://doi.org/10.1089/jir.2010.0019" @default.
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