Interactions between bacterial CpG-DNA and TLR9 bridge innate and adaptive immunity

Curr Opin Microbiol. 2002 Feb;5(1):62-9. doi: 10.1016/s1369-5274(02)00287-4.

Abstract

The astounding adjuvanticity and Th1-polarizing immunobiology of bacterial CpG-DNA and mimicking CpG-oligonucleotides continue to mirror promising therapeutic potential. The past year has witnessed some particularly impressive progress in knowledge of its molecular mode of action. Accordingly, CpG-DNA acts as a "pathogen-associated" molecular pattern that is recognized by TLR9 expressed, in particular, by dendritic cells. Interactions between CpG-DNA and TLR9 rapidly activate antigen-presenting dendritic cells through the ancient Toll/IL-1-receptor signaling pathway to upregulate co-stimulatory molecules and to produce Th1-polarizing cytokines, such as interleukin-12 and interleukin-18. Thus, interactions between CpG-DNA and TLR9 effectively bridge innate and acquired immunity.

Publication types

  • Research Support, Non-U.S. Gov't
  • Review

MeSH terms

  • Animals
  • Bacteria / metabolism
  • Bacteria / pathogenicity*
  • Bacterial Infections / immunology
  • Bacterial Proteins / metabolism
  • CpG Islands / physiology*
  • DNA, Bacterial / metabolism
  • DNA-Binding Proteins / metabolism*
  • Dendritic Cells / immunology
  • Dendritic Cells / metabolism
  • Drosophila Proteins*
  • Gene Expression
  • Humans
  • Immunity, Active / physiology*
  • Immunity, Innate / physiology*
  • Ligands
  • Membrane Glycoproteins / metabolism
  • Mice
  • Receptors, Cell Surface / metabolism*
  • Signal Transduction / genetics
  • Toll-Like Receptor 9
  • Toll-Like Receptors

Substances

  • Bacterial Proteins
  • DNA, Bacterial
  • DNA-Binding Proteins
  • Drosophila Proteins
  • Ligands
  • Membrane Glycoproteins
  • Receptors, Cell Surface
  • TLR9 protein, human
  • Tlr9 protein, mouse
  • Toll-Like Receptor 9
  • Toll-Like Receptors