Impairment of T-regulatory cells in cord blood of atopic mothers

    loading  Checking for direct PDF access through Ovid

Abstract

Background:

Maternal atopy is a strong predictor for the development of childhood allergic diseases. The underlying mechanisms are ill defined, yet regulatory T (Treg) and TH17 cells may play a key role potentially shaping the early immune system toward a proallergic or antiallergic immune regulation.

Objective:

We examined TH1/TH2, Treg, and TH17 cell responses to innate (lipid A/peptidoglycan) and mitogen/adaptive (phytohemagglutinin/Dermatophagoides pteronyssinus1) immune stimulation in cord blood from offspring of atopic/nonatopic mothers.

Methods:

Cord blood mononuclear cells from 161 healthy neonates (59% nonatopic, 41% atopic mothers) were investigated regarding Treg and TH17 cells (mRNA/surface markers), suppressive function, and proliferation/cytokine secretion.

Results:

Cord blood from offspring of atopic mothers showed fewer innate-induced Treg cells (CD4+CD25+high), lower mRNA expression of associated markers (glucocorticoid-induced tumor necrosis factor receptor–related protein/lymphocyte activation gene 3;P< .05), and a trend toward lower Forkhead box transcription factor 3 (Foxp3) expression. Treg cell function was impaired in mitogen-induced suppression of T effector cells in cord blood of offspring from atopic mothers (P= .03). Furthermore, IL-10 and IFN-γ secretion were decreased in innate-stimulated cord blood of offspring from atopic mothers (P= .04/.05). Innate-induced IL-17 was independent of maternal atopy and highly correlated with IL-13 secretion.

Conclusion:

In offspring of atopic mothers, Treg cell numbers, expression, and function were impaired at birth. TH17 cells were correlated with TH2 cells, independently of maternal atopy.

Related Topics

    loading  Loading Related Articles