Nature Immunology2, 947 - 950 (2001)
Published online: 4 September 2001; | doi:10.1038/ni712
Toll-like receptors control activation of adaptive immune responses
Markus Schnare1, 2, 4, Gregory M. Barton1, 2, 4, Agnieszka Czopik Holt1, Kiyoshi Takeda3, Shizuo Akira3
& Ruslan Medzhitov1, 2
1
Section of Immunobiology, Yale University School of Medicine, New Haven, CT 06520, USA.
2
Howard Hughes Medical Institute, New Haven, CT 06520, USA.
3
Department of Host Defense, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka 565-0871, Japan.
4
These authors contributed equally to this work.
Correspondence should be addressed to Ruslan Medzhitov ruslan@yale.edu
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-B 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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B 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.
