Format

Send to

Choose Destination
Cell Mol Immunol. 2013 May;10(3):253-60. doi: 10.1038/cmi.2012.78. Epub 2013 Mar 25.

Vγ9Vδ2-T lymphocytes have impaired antiviral function in small-for-gestational-age and preterm neonates.

Author information

1
The Joint Research Center of West China Second University Hospital of Sichuan University and Faculty of Medicine of the University of Hong Kong, Chengdu, China.

Abstract

Preterm and small-for-gestational-age (SGA) neonates are vulnerable groups that are susceptible to various microbial infections. Vγ9Vδ2-T cells are critical components of the host immune system and have been demonstrated to play an important role in the defense against viral infection in adults. However, the characteristics of Vγ9Vδ2-T cells in children, especially the preterm and SGA populations, are poorly understood. Here, we examined the frequency and antiviral function of Vγ9Vδ2-T cells in neonates, including preterm, SGA and full-term babies. When compared to adults, neonates had a significantly lower percentage of Vγ9Vδ2-T cells in the blood. Upon influenza virus stimulation, neonatal Vγ9Vδ2-T cells, especially from preterm and SGA babies, showed markedly decreased and delayed antiviral cytokine responses than those of adults. In addition, the antiviral responses of neonatal Vγ9Vδ2-T cells were positively correlated with gestational age and birth weight. Finally, a weaker expansion of Vγ9Vδ2-T cells by isopentenyl pyrophosphate (IPP) was shown in neonates than the expansion in adults. Our data suggest that the depressed antiviral activity and decreased frequency of Vγ9Vδ2-T cells may likely account for the high susceptibility to microbial infection in neonates, particularly in preterm and SGA babies. Improving Vγ9Vδ2-T-cell function of neonates may provide a new way to defend against virus infection.

PMID:
23524656
PMCID:
PMC4012779
DOI:
10.1038/cmi.2012.78
[Indexed for MEDLINE]
Free PMC Article

Supplemental Content

Full text links

Icon for Nature Publishing Group Icon for PubMed Central
Loading ...
Support Center