Read the summary and the most important questions on L7-8 II: Intestinal Immunity II | Jerry Wells

• 1 TLR

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• Why do TLR1-2 and TLR2-6 bind to each other?

  It will yield the highest affinity in binding the lipid chain of microbes.

• What does TLR2-6 bind?  

  Lipoteichoic acid (LTA), in cell wall of Gram+ bact.

• How does TLR2-6 bind?

  Lipid chains in LTA bind to TLR2, the head group contacts TLR6 to form an active heterodimer.

• How is LPS build up?

  Variable O-specific chain: used for identification
  Conserved core region
  Conserved Lipid A, which binds to TLR4

• What is the cascade of LPS binding to TLR4?

  LPS binds to LBP (LPS-binding protein)
  Interacts with CD14
  LPS binds to TLR4 monomer with MD2 co-receptor
  TLR4 receptor dimerization: MyD88 -> early NF-kB
  Internalization: late NF-kB and type I IFNs

• What is the signalling pathway for extracellular TLR4/5/9?

  MyD88 --> phosphorylation of IKB (degradation of NF-kB inhibitor)
  NF-kB into nucleus -> Type 1 IFN/infl. cytokines en chemokines

• What is the signalling pathway of endosomal TLR3/4?

  Via TRIF, two ways:
  Type 1 IFN in nucleus
  via NF-kB into nucleus: inflammation cytokines and chemokines

• 2 Epithelial cells

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• What is the polarisation of eptihelial cells, and how is it maintained?

  Due to tight junctions, different receptors/structures are either present on the basolateral or apical surface.

• How does polarization aid epithelial function?

  It allows the gut to be permeable, yet still forms a barrier vs. pathogens.

• How is TLR9 distributed over an epithelial cell, and where will it lead to IL-8 production?

  TLR9 (CpG DNA) is present both apical and basolateral, but it only activates IL-8 production on the BL side.