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Altered Toll-Like Receptor Signalling in Children with Down Syndrome.

Dean Huggard1,2,3,4, W J Koay1, Lynne Kelly1,2

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|October 16, 2019
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Summary

Toll-like receptor 2 (TLR2) signaling is dysregulated in children with Down syndrome (DS), showing increased TLR2 expression and altered immune gene expression. Sparstolonin B effectively reduced inflammation, suggesting therapeutic potential for DS.

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Area of Science:

  • Immunology
  • Genetics
  • Pediatrics

Background:

  • Toll-like receptors (TLRs) initiate innate immunity, with TLR2 recognizing gram-positive bacteria and linked to chronic inflammation.
  • Children with Down syndrome (DS) face increased infection risk and autoimmunity, suggesting potential immune dysregulation.
  • Sparstolonin B (SsnB) is a TLR antagonist that reduces cytokine production and improves sepsis outcomes.

Purpose of the Study:

  • To investigate potential abnormalities in Toll-like receptor (TLR) signaling pathways in children with Down syndrome (DS).
  • To evaluate the expression of TLR2 and key TLR signaling proteins (MyD88, IRAK4, TRIF) in DS.
  • To assess the efficacy of Sparstolonin B (SsnB) in modulating TLR responses and cytokine production in DS.

Main Methods:

  • Flow cytometry was used to determine TLR2 expression on neutrophils and monocytes.
  • Quantitative PCR measured gene expression of MyD88, IRAK4, and TRIF.
  • ELISA assessed cytokine production following stimulation with LPS, Pam3Csk4, and treatment with SsnB.

Main Results:

  • Children with DS exhibited significantly increased TLR2 expression on neutrophils and monocytes compared to controls.
  • Baseline MyD88 expression was lower, while TRIF expression was higher in children with DS.
  • SsnB effectively reduced TLR2 and CD11b expression and abrogated cytokine production in both groups.

Conclusions:

  • TLR signaling, particularly the TLR2 pathway, is dysregulated in children with Down syndrome, potentially contributing to chronic inflammation.
  • The observed immune dysregulation in DS involves altered expression of TLR2 and associated signaling molecules.
  • Sparstolonin B demonstrates potential as a therapeutic agent by attenuating pro-inflammatory mediators in DS.