金黄色葡萄球菌通过 IL-10、PD-L1 和 TLR2 控制适应性免疫反应。
Control of adaptive immune responses by Staphylococcus aureus through IL-10, PD-L1, and TLR2.
机构信息
Laboratory of Immunology, Division of Therapeutic Proteins, Office of Biotechnology Products, Center for Drug Evaluation and Research , Food and Drug Administration, Bethesda, MD 20892, USA.
出版信息
Sci Rep. 2012;2:606. doi: 10.1038/srep00606. Epub 2012 Aug 28.
Microbes induce innate immune responses in hosts. It is critical to know how different microbes control adaptive responses through innate pathways. The impact of gram-positive bacteria on the innate and adaptive responses is unclear. Herein we report that Staphylococcus aureus induces IL-10, Th17-inducing cytokines IL-6 and IL-23, chemokines, and regulates dendritic cell markers. S. aureus inhibits T-cell IL-2 responses through modulation of HLA-DR, CD86 and PD-L1. IFN-gamma, Src kinase inhibitors, or TLR2 antibodies prevented the down-modulation of HLA-DR by S. aureus. Our data demonstrate that innate TLR signaling induces multi-dimensional inhibition of adaptive immune responses, which may contribute to the lack of protective immunity to bacteria or microbe tolerance. IL-10 and PD-L1 antagonists may boost immunity to vaccines for S. aureus and other microbes.
微生物在宿主中诱导先天免疫反应。了解不同微生物如何通过先天途径控制适应性反应至关重要。革兰氏阳性菌对先天和适应性反应的影响尚不清楚。本文报告金黄色葡萄球菌诱导 IL-10、Th17 诱导细胞因子 IL-6 和 IL-23、趋化因子，并调节树突状细胞标志物。金黄色葡萄球菌通过调节 HLA-DR、CD86 和 PD-L1 抑制 T 细胞 IL-2 反应。IFN-γ、Src 激酶抑制剂或 TLR2 抗体可防止金黄色葡萄球菌下调 HLA-DR。我们的数据表明，先天 TLR 信号诱导适应性免疫反应的多维抑制，这可能导致对细菌或微生物耐受缺乏保护性免疫。IL-10 和 PD-L1 拮抗剂可能增强对金黄色葡萄球菌和其他微生物疫苗的免疫力。
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