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Single-Stranded Nucleic Acids Regulate TLR3/4/7 Activation through Interference with Clathrin-Mediated Endocytosis.

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Extracellular single-stranded oligonucleotides (ssON) inhibit endocytosis, dampening Toll-like receptor (TLR) signaling. This process, called SOMIE, helps prevent excessive immune responses to pathogens.

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Area of Science:

  • Immunology
  • Cell Biology
  • Molecular Biology

Background:

  • Endosomal Toll-like receptors (TLRs) are crucial for pathogen recognition.
  • Tight regulation of TLR signaling is necessary to prevent excessive inflammation.
  • Mechanisms controlling TLR regulatory pathways remain largely unknown.

Purpose of the Study:

  • To investigate the regulatory mechanisms of endosomal TLR signaling.
  • To identify factors that control immune responses mediated by TLRs.
  • To elucidate the role of extracellular nucleic acids in immune regulation.

Main Methods:

  • Investigated the effect of single-stranded oligonucleotides (ssON) on endocytic pathways.
  • Assessed ssON concentration and length dependence for endocytic inhibition.
  • Analyzed modulation of TLR3/4/7 signaling downstream of affected endosomes.
  • Evaluated ssON effects on dsRNA-mediated inflammation in non-human primates.

Main Results:

  • Single-stranded oligonucleotides (ssON), including ssDNA and ssRNA, inhibit endocytic pathways.
  • This inhibition is concentration-dependent and requires a minimum ssON length.
  • ssON interfere with signaling downstream of TLRs within affected endosomes.
  • ssON injection reduces dsRNA-induced inflammatory responses in primate skin.

Conclusions:

  • Extracellular ssON play a regulatory role in the endocytic uptake of TLR ligands.
  • ssON-mediated interference of endocytosis (SOMIE) temporarily dampens TLR3/4/7 signaling.
  • SOMIE provides a mechanism to avert excessive immune responses, preventing harmful inflammation.