Toll-like receptors control activation of adaptive immune responses

被引:1123
作者
Schnare, M
Barton, GM
Holt, AC
Takeda, K
Akira, S
Medzhitov, R [1 ]
机构
[1] Yale Univ, Sch Med, Immunol Sect, New Haven, CT 06520 USA
[2] Howard Hughes Med Inst, New Haven, CT 06520 USA
[3] Osaka Univ, Microbial Dis Res Inst, Dept Host Def, Suita, Osaka 5650871, Japan
关键词
D O I
10.1038/ni712
中图分类号
R392 [医学免疫学]; Q939.91 [免疫学];
学科分类号
100102 [免疫学];
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 (T(H)1) but not T(H)2 immune responses. These results suggest that distinct pathways of the innate immune system control activation of the two effector arms of adaptive immunity.
引用
收藏
页码:947 / 950
页数:4
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