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标题:Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk.
时间:2018-10-11 17:13:42
DOI:10.1038/ni.2015
PMID:21441935
大小:1118 kb
页数:11 PAGES
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目录:
  • Intracellular MHC class II molecules promote TLR-triggered innate immune responses by maintaining activation of the kinase Btk
    • RESULTS
      • H2 deficiency protects mice from LPS and bacterial challenge
      • Impaired cytokine production in TLR-triggered H2−/− APCs
      • Impaired TLR signaling in H2−/− macrophages
      • MHC class II molecules maintain TLR-triggered Btk activation
      • Intracellular MHC class II molecules bind Btk via CD40
      • Binding of Btk with CD40 is required for full TLR response
      • Btk enhances TLR signaling by binding MyD88 and TRIF
    • DISCUSSION
    • Methods
    • ONLINE METHODS
      • Mice and reagents.
      • Plasmid constructs.
      • Cell culture and transfection.
      • RNA-mediated interference.
      • Cytokine detection.
      • RNA quantification.
      • Assay of luciferase reporter gene expression.
      • Immunoprecipitation and immunoblot analysis.
      • Nanospray liquid chromatography–tandem mass spectrometry.
      • In vitro kinase assay.
      • Confocal microscopy.
      • Establishment of endotoxin shock model and bacterial sepsis model.
      • Bone marrow transplantation.
      • Macrophage reconstitution.
      • Statistical analysis.
    • Acknowledgments
    • AUTHOR CONTRIBUTIONS
    • COMPETING FINANCIAL INTERESTS
    • References
    • Figure 1 Deficiency in MHC class II protects mice from challenge with TLR ligands.
    • Figure 2 Deficiency in MHC class II protects mice from sepsis induced by live E.
    • Figure 3 Deficiency in MHC class II attenuates TLR-triggered production of proinflammatory cytokines and type I interferon in macrophages and DCs.
    • Figure 4 Deficiency in MHC class II impairs the MyD88-dependent and TRIF-dependent activation of mitogen-activated protein kinases, NF-κB, IRF3 and IRF7 in TLR-triggered macrophages.
    • Figure 5 MHC class II molecules promote TLR-triggered inflammatory innate responses by maintaining Btk activation.
    • Figure 6 Intracellular MHC class II molecules interact with CD40 and Btk.
    • Figure 7 Activated Btk interacts with MyD88 and TRIF, promoting the activation of MyD88-dependent and TRIF-dependent pathways.

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