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      A novel Toll-like receptor that recognizes vesicular stomatitis virus.

      The Journal of Biological Chemistry
      Animals, Cloning, Molecular, Gene Knockdown Techniques, Interferon Regulatory Factor-7, genetics, immunology, metabolism, Interferon Type I, MAP Kinase Kinase Kinases, Mice, Mice, Knockout, Myeloid Differentiation Factor 88, NF-kappa B, NIH 3T3 Cells, Rhabdoviridae Infections, Signal Transduction, Toll-Like Receptors, Vesiculovirus

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          Abstract

          Toll-like receptors (TLRs) are the key molecular sensors used by the mammalian innate immune system to detect various types of pathogens. Tlr13 is a novel and uncharacterized member of the mammalian TLR family. Here we report the cloning and characterization of tlr13. Tlr13 is predominantly expressed in the spleen, particularly in dendritic cells and macrophages. Tlr13 appears to activate a MyD88- and TAK1-dependent TLR signaling pathway, inducing the activation of NF-κB. This receptor can also activate type 1 interferon through IRF7. Furthermore, Tlr13 seems to be another intracellular TLR. Remarkably, cells expressing tlr13 fail to respond to known TLR ligands but instead respond specifically to vesicular stomatitis virus. Cells with the knockdown of tlr13 are highly susceptible to vesicular stomatitis virus infection. Thus, these results provide an important insight into the potential role of the novel Toll-like receptor tlr13 in the recognition of viral infection.

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