Journal
PEDIATRIC RESEARCH
Volume 71, Issue 2, Pages 136-143Publisher
NATURE PUBLISHING GROUP
DOI: 10.1038/pr.2011.26
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Funding
- Rainbow Babies and Children's Foundation
- NICHD Research Career Development in Child Health [K12 HD057581]
- Case Western Reserve University Center for AIDS Research [AI-36219]
- National Institutes of Health [AI-076174]
- Tampa General Hospital Office of Clinical Research
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INTRODUCTION: Inflammation and infection are associated with premature birth and with activation of the fetal immune system. We hypothesized that exposure to microbial Toll-like receptor (TLR) ligands plays an important role in neonatal T-cell maturation and that early exposure to microbial products may result in early T-cell maturation and a tendency for these matured effector cells to change their homing receptor patterns. RESULTS: Expression of the CD45RO marker was induced in term neonatal T cells after in vitro exposure to TLR ligands for 7 days. Interestingly, naive T cells from adult blood were unaffected by TLR ligand exposure. In addition, neonatal T cells had more cells with decreased expression of the alpha 4 beta 7 integrins and increased expression of CCR4 after in vitro exposure of TLR ligands-similar to the expression of these molecules in adult naive T cells. DISCUSSION: These findings are relevant for the understanding of neonatal T-cell maturation and may contribute to our understanding of multiorgan inflammatory complications of prematurity. METHODS: Cord blood was obtained from term and preterm infants. Using flow cytometry, we identified a mature (CD45RO(+)) phenotype in preterm infant cord blood (CB) T cells that had decreased expression of the alpha 4 beta 7 integrins and increased expression of the C-C chemokine receptor 4 (CCR4) as compared with term infant CB.
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