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

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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.


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.


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.


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.


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.

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