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Characterization of regulatory T cells in urban newborns
Ngoc P Ly1, Begona Ruiz-Perez, Rachel M McLoughlin
1Pediatric Pulmonary Medicine, University of California San Francisco Children's Hospital and UCSF Medical School, San Francisco, CA, USA. lyn@peds.ucsf.edu.
Insights
Newborns in urban areas have immature T regulatory (Treg) cells, impacting their immune function. This study compared Treg cells in urban newborns and their mothers, revealing functional deficits in infants that may influence asthma risk.
Area of Science:
- Immunology
- Pediatrics
- Environmental Health
Background:
- Asthma prevalence is high in US urban children.
- Impaired T regulatory (Treg) cells at birth may contribute to asthma development in urban infants.
- The study investigated Treg cells in urban newborns and their mothers.
Purpose of the Study:
- To compare the phenotype and function of Treg cells in the cord blood of urban newborns with those in the peripheral blood of their mothers.
- To identify potential immune mechanisms underlying asthma risk in urban children.
Main Methods:
- Quantified Treg cell numbers, expression of markers (CD45RA, CD45RO, CD69, HLA-DR), and suppressive function in urban newborns and mothers.
- Utilized flow cytometry to analyze Treg cell populations.
- Assessed Treg suppressive capacity by measuring lymphocyte proliferation.
Main Results:
- Newborns had similar FOXP3+ cell counts but fewer CD4+CD25+bright cells compared to mothers.
- Newborn Treg cells showed a naive (CD45RA+) phenotype, unlike the activated/memory phenotype in mothers.
- Newborns exhibited reduced TGF-beta production and impaired Treg suppression of lymphocyte proliferation.
Conclusions:
- U.S. urban newborns possess Treg cells with an immature phenotype and reduced function compared to their mothers.
- These findings suggest potential immune dysregulation at birth in urban infants.
- Further longitudinal studies are necessary to understand Treg cell maturation and its link to atopic disease risk.
Background:
In the United States, asthma prevalence is particularly high among urban children. Although the underlying immune mechanism contributing to asthma has not been identified, having impaired T regulatory (Treg) cells at birth may be a determining factor in urban children. The objective of this study was to compare Treg phenotype and function in cord blood (CB) of newborns to those in peripheral blood (PB) of a subset of participating mothers.
Methods:
Treg numbers, expression, and suppressive function were quantified in subjects recruited prenatally from neighborhoods where >/= 20% of families have incomes below the poverty line. Proportion of Treg cells and expression of naïve (CD45RA) or activated (CD45RO, CD69, and HLA-DR) markers in CD4+T cells was measured by flow cytometry. Treg suppressive capacity was determined by quantifying PHA-stimulated lymphocyte proliferation in mononuclear cell samples with and without CD25 depletion.
Results:
In an urban cohort of 119 newborns and 82 mothers, we found that newborns had similar number of cells expressing FOXP3 as compared to the mothers but had reduced numbers of CD4+CD25+bright cells that predominantly expressed the naïve (CD45RA) rather than the activated/memory (CD45RO) phenotype found in the mothers. Additionally, the newborns had reduced mononuclear cell TGF-beta production, and reduced Treg suppression of PHA-stimulated lymphocyte proliferation compared to the mothers.
Conclusion:
U.S. urban newborns have Treg cells that express FOXP3, albeit with an immature phenotype and function as compared to the mothers. Longitudinal follow-up is needed to delineate Treg cell maturation and subsequent risk for atopic diseases in this urban birth cohort.
