HERV-K and W expression in peripheral mononuclear cells of children with Henoch-Schönlein purpura and relation with TLR activation

Minerva Pediatr (Torino). 2022 Aug;74(4):421-427. doi: 10.23736/S2724-5276.17.04717-X. Epub 2017 May 4.

Abstract

Background: HERVs expression seems impaired in several diseases, ranging from autoimmune to neoplastic disorders. However, various stimuli may re-activate HERVs transcription. Henoch-Schönlein purpura is the most common cause of vasculitis in children. The role of microbial antigens in the pathogenesis of HSP remains elusive. Toll-like receptors (TLRs) are the first line of defense for the host to initiate an immune and inflammatory response. We aimed to investigate HERV, K and W expression in peripheral mononuclear cells of children with HSP and relation with TLRs activation.

Methods: The study enrolled 63 children affected by HSP. We used RT-PCR to detect GAPDH in the peripheral blood mononuclear cells samples to normalize the data. Subsequently, the viral pol gene HERVs and TLRs transcripts in the same samples were assessed.

Results: HERV K and W was expressed in all samples analyzed but the level of expression was much lower in the HSP that in HC P=0.0006 and P=0.0004 for HERV-K and -W respectively. TLR2 was hyper-expressed in 39 vs. 63 (62%) of the HSP, TLR3 in 23 vs. 63 (42%), TLR4 in 42 vs. 63 (66%) and TLR9 in 32 vs. 63 (52%). The different expression was statistically significant only for TLR4 (P=0.0276) no for TLR2,3 and 9 (P=0.1251; 0.3964 and 0.1882 respectively). Spearman's test demonstrated no correlation between the low expression of HERV-K and HERV-W and high expression of TLRs.

Conclusions: The results of the present study demonstrated that mRNA expression of HERV-K and -W and TLRs did not directly correlated.

MeSH terms

  • Child
  • Endogenous Retroviruses* / genetics
  • Endogenous Retroviruses* / metabolism
  • Humans
  • IgA Vasculitis* / genetics
  • Leukocytes, Mononuclear / metabolism
  • Leukocytes, Mononuclear / virology
  • Toll-Like Receptor 2 / genetics
  • Toll-Like Receptor 2 / metabolism
  • Toll-Like Receptor 3
  • Toll-Like Receptor 4 / genetics
  • Toll-Like Receptor 4 / metabolism
  • Toll-Like Receptor 9
  • Toll-Like Receptors* / genetics
  • Toll-Like Receptors* / metabolism

Substances

  • TLR2 protein, human
  • TLR3 protein, human
  • TLR4 protein, human
  • TLR9 protein, human
  • Toll-Like Receptor 2
  • Toll-Like Receptor 3
  • Toll-Like Receptor 4
  • Toll-Like Receptor 9
  • Toll-Like Receptors