Regulatory T cell frequencies are increased in preterm infants with clinical early-onset sepsis

Clin Exp Immunol. 2016 Aug;185(2):219-27. doi: 10.1111/cei.12810. Epub 2016 Jun 12.

Abstract

The predisposition of preterm neonates to invasive infection is, as yet, incompletely understood. Regulatory T cells (Tregs ) are potential candidates for the ontogenetic control of immune activation and tissue damage in preterm infants. It was the aim of our study to characterize lymphocyte subsets and in particular CD4(+) CD25(+) forkhead box protein 3 (FoxP3)(+) Tregs in peripheral blood of well-phenotyped preterm infants (n = 117; 23 + 0 - 36 + 6 weeks of gestational age) in the first 3 days of life in comparison to term infants and adults. We demonstrated a negative correlation of Treg frequencies and gestational age. Tregs were increased in blood samples of preterm infants compared to term infants and adults. Notably, we found an increased Treg frequency in preterm infants with clinical early-onset sepsis while cause of preterm delivery, e.g. chorioamnionitis, did not affect Treg frequencies. Our data suggest that Tregs apparently play an important role in maintaining maternal-fetal tolerance, which turns into an increased sepsis risk after preterm delivery. Functional analyses are needed in order to elucidate whether Tregs have potential as future target for diagnostics and therapeutics.

Keywords: FoxP3; amniotic infection; early-onset sepsis; preterm infants; regulatory T cells.

Publication types

  • Observational Study

MeSH terms

  • Adult
  • Amnion / microbiology
  • Chorioamnionitis / immunology
  • Female
  • Forkhead Transcription Factors / blood
  • Gestational Age
  • Humans
  • Immune Tolerance
  • Infant
  • Infant, Newborn
  • Infant, Premature / immunology*
  • Infant, Premature, Diseases / immunology*
  • Lymphocyte Subsets / cytology
  • Lymphocyte Subsets / immunology
  • Pregnancy
  • Sepsis / immunology*
  • Sepsis / microbiology
  • T-Lymphocytes, Regulatory / immunology*

Substances

  • FOXP3 protein, human
  • Forkhead Transcription Factors