Toll-like receptors control activation of adaptive immune responses.
摘要：
Mechanisms that control the activation of antigen-specific immune responses in vivo are poorly understood. It has been suggested that the initiation of adaptive immune responses is controlled by innate immune recognition. Mammalian Toll-like receptors play an essential role in innate immunity by recognizing conserved pathogen-associated molecular patterns and initiating the activation of NF-kappaB and other signaling pathways through the adapter protein, MyD88. Here we show that MyD88-deficient mice have a profound defect in the activation of antigen-specific T helper type 1 (TH1) but not TH2 immune responses. These results suggest that distinct pathways of the innate immune system control activation of the two effector arms of adaptive immunity.
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关键词：
Animals Mice, Knockout Mice Dendritic Cells Th1 Cells Cells, Cultured Adaptor Proteins, Signal Transducing Membrane Glycoproteins Drosophila Proteins Receptors, Cell Surface
DOI：
10.1038/ni712
被引量：
年份：
2001
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