Effects of intrauterine exposure to maternal-derived HBeAg on T cell immunity in cord blood.

Immature immune system and immune tolerance induced by exposure to HBeAg in utero and/or shortly after infection in newborns were reportedly the causes of chronic HBV infection. To investigate the effect of maternal-derived HBeAg on neonatal T cell immunity, we analysed and compared T cell phenotypes and functions among neonates born to HBsAg(+)/HBeAg(+)mothers (HBeAg(+)neonates), HBsAg(+)/HBeAg(-)mothers (HBeAg(-)neonates) and healthy control mothers (HC neonates), using flow cytometry. The results showed that neonatal T cell phenotypes were similar regardless of HBeAg exposure. Upon anti-CD3 and anti-CD28 stimulation in HBeAg(+)neonates, CD4(+)T cell production of IFN-gamma (P < .05) was significantly enhanced, while CD8(+)T cells secreted significantly more IL-2 compared with those in HBeAg(-)and HC groups (P < .05). Moreover, similar levels of IFN-gamma and IL-10 were observed in the culture supernatant after stimulation with rHBsAg, rHBcAg or rHBeAg among HBeAg+, HBeAg(-)and HC neonates, whereas HBeAg(+)neonates produced more TNF-alpha than HBeAg(-)neonates upon stimulation with rHBcAg. In conclusion, the results indicated that the HBsAg(+)/HBeAg(+)maternal environment did not influence the phenotypes of cord blood T cells but boosted neonatal non-specific Th1-type cytokine production.