Abstract
Intrauterine environmental exposures have been shown to influence neonatal immunity and subsequent atopy. The effect of “pro-allergic” TH2 cytokines on neonatal cord blood (CB) hematopoietic progenitor cells, the phenotype and differentiation of which are associated with atopic risk, is currently unknown. Since we have previously shown that high-atopic risk infants have decreased eosinophil-basophil (Eo/B) differentiation after stimulation with LPS, we investigated whether a TH2 milieu (IL-4 or IL-13) could influence LPS-induced Eo/B colony forming units (CFU), and the mechanism(s) through which this might occur.
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