Abstract
The concept that Toll-like receptors (TLRs) recognize specific molecular patterns in various pathogens has been established. In signal transduction via TLRs, MyD88, which harbors a Toll/IL-1 receptor (TIR)-domain and a death domain, has been shown to link between TLRs and MyD88-dependent downstream events leading to proinflammatory cytokine production and splenocyte proliferation. However, recent studies using MyD88-deficient mice have revealed that some TLRs possess a MyD88-independent pathway, which is represented by interferon (IFN)-beta production induced by LPS stimulation. This indicates that additional signaling molecules other than MyD88 exist in the TLR signaling pathway. Indeed, two additional TIR domain-containing adaptors, TIRAP/Mal and TRIF, have recently been identified. Both define the specific biological responses of each TLR.
Publication types
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Research Support, Non-U.S. Gov't
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Review
MeSH terms
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Adaptor Proteins, Signal Transducing
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Adaptor Proteins, Vesicular Transport / genetics*
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Adaptor Proteins, Vesicular Transport / metabolism
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Animals
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Antigens, Differentiation / metabolism*
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Membrane Glycoproteins / genetics*
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Membrane Glycoproteins / metabolism*
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Mice
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Mice, Knockout
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Myeloid Differentiation Factor 88
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Protein Structure, Tertiary
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Receptors, Cell Surface / metabolism*
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Receptors, Immunologic / metabolism*
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Receptors, Interleukin-1 / genetics*
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Receptors, Interleukin-1 / metabolism
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Signal Transduction / physiology*
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Toll-Like Receptors
Substances
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Adaptor Proteins, Signal Transducing
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Adaptor Proteins, Vesicular Transport
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Antigens, Differentiation
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Membrane Glycoproteins
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Myd88 protein, mouse
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Myeloid Differentiation Factor 88
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Receptors, Cell Surface
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Receptors, Immunologic
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Receptors, Interleukin-1
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TICAM-1 protein, mouse
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TIRAP protein, mouse
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Toll-Like Receptors