期刊
SCIENCE
卷 309, 期 5739, 页码 1380-1384出版社
AMER ASSOC ADVANCEMENT SCIENCE
DOI: 10.1126/science.1113401
关键词
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资金
- NCI NIH HHS [P01CA94237, R01CA101795, P50CA58204, P50 CA093459, R01CA90327] Funding Source: Medline
CD4(+) regulatory T (Treg) cells have a profound ability to suppress host immune responses, yet little is understood about how these cells are regulated. We describe a mechanism [inking Toll-like receptor (TLR) 8 signaling to the control of Treg cell function, in which synthetic and natural ligands for human TLR8 can reverse Treg cell function. This effect was independent of dendritic cells but required functional TLR8-MYD88-IRAK4 signaling in Treg cells. Adoptive transfer of TLR8 ligand-stimulated Treg cells into tumor-bearing mice enhanced antitumor immunity. These results suggest that TLR8 signaling could play a critical role in controlling immune responses to cancer and other diseases.
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