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Assessing the Development of Murine Plasmacytoid Dendritic Cells in Peyer's Patches Using Adoptive Transfer of Hematopoietic Progenitors
Published on: March 17, 2014
Blood plasmacytoid dendritic cell responses to CpG oligodeoxynucleotides are impaired in human newborns
Dominique De Wit1, Véronique Olislagers, Stanislas Goriely
1Hôpital Erasme-Department of Immunology, 808, Route de Lennik, B-1070 Brussels, Belgium.
Insights
Neonatal plasmacytoid dendritic cells (pDCs) show impaired interferon-alpha (IFN-alpha) production in response to CpG, suggesting a potential vulnerability in newborns to infections and impacting CpG adjuvant use.
Area of Science:
- Immunology
- Neonatal Immunology
Background:
- Plasmacytoid dendritic cells (pDCs) are crucial immune cells that recognize pathogen-associated molecular patterns.
- CpG motifs in bacterial DNA activate pDCs, stimulating immune responses.
- Neonatal immune system immaturity contributes to increased susceptibility to infections.
Purpose of the Study:
- To investigate the functional capacity of pDCs in human newborns compared to adults.
- To assess CpG-induced interferon-alpha (IFN-alpha) production and pDC maturation in neonates.
- To understand the implications for neonatal immunity and vaccine adjuvant strategies.
Main Methods:
- Comparison of pDC function in cord blood (neonates) and adult blood.
- Stimulation with specific CpG oligodeoxynucleotides (CpG 2216 for IFN-alpha, CpG 2006 for maturation).
- Analysis of cell surface marker expression (CD80, CD83, CD86, CD40, HLA-DR, CD54) and IFN-alpha production at protein and mRNA levels.
Main Results:
- Neonatal pDCs exhibited reduced upregulation of maturation markers (CD80, CD83, CD86, CD40) but not HLA-DR or CD54.
- CpG-induced IFN-alpha production was significantly impaired in neonatal blood, at both protein and mRNA levels.
- This defect in IFN-alpha production was intrinsic to pDCs and persisted for at least four days after birth.
Conclusions:
- Human newborns possess intrinsically deficient pDCs regarding CpG-induced IFN-alpha production.
- This neonatal immune defect may explain increased susceptibility to infections in newborns.
- Findings suggest caution regarding the use of CpG oligodeoxynucleotides as vaccine adjuvants in the neonatal period.
Abstract:
Plasmacytoid dendritic cells (pDCs) respond to unmethylated cytosine-phosphate-guanosine (CpG) motifs present in bacterial DNA or unmethylated synthetic oligodeoxynucleotides (CpG). In order to assess the function of pDCs in human newborns, interferon-alpha (IFN-alpha) production induced by CpG 2216 and phenotypic maturation of pDCs in response to CpG 2006 were compared in cord blood and adult blood. We first observed that neonatal pDCs displayed decreased up-regulation of CD80, CD83, CD86, and CD40, whereas HLA-DR and CD54 up-regulation did not differ significantly between adults and neonates. We then found that the production of IFN-alpha in response to CpG was dramatically impaired in cord blood. This neonatal defect was detected both at protein and mRNA levels and was still present in blood of 4-day-old babies. Further experiments on enriched pDCs confirmed that these cells are intrinsically deficient in CpG-induced IFN-alpha production at birth. These findings might be relevant to the increased susceptibility of human newborns to infections as well as to the use of CpG oligodeoxynucleotides as vaccine adjuvants in the neonatal period.
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