Effects of intrauterine exposure to maternal-derived HBeAg on T cell immunity in cord blood
Effects of intrauterine exposure to maternal-derived HBeAg on T cell immunity in cord blood
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宫内暴露于母源性 HBeAg 对脐带血 T 细胞免疫的影响
DOI：
10.1111/sji.12914
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发表时间：
2020-06-29
影响因子：
3.7
通讯作者：
Liu, Zhihua
中科院分区：
文献类型：
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作者：
Huang, Meiting;Gao, Yunfei;Liu, Zhihua
新生儿宫内和(或)感染后不久暴露于HBeAg诱导的免疫系统不成熟和免疫耐受是导致慢性乙肝感染的主要原因。为探讨母源性HBeAg对新生儿T细胞免疫功能的影响，应用流式细胞术分析比较了HBeAg(+)/HBeAg(+)母亲(HBeAg(+)新生儿)、HBeAg(+/HBeAg(-)母亲(HBeAg(-)新生儿)和健康对照母亲(HC新生儿)所生新生儿的T细胞表型和功能。结果显示，无论HBeAg暴露与否，新生儿T细胞表型相似。HBeAg(+)组新生儿经抗CD3和抗CD28刺激后，CD8(+)T细胞分泌IL-2的量显著高于HBeAg(-)组和HC组(P<0.05)。经rHBs Ag、rHBcAg或rHBeAg刺激后，HBeAg+、HBeAg(-)和HC新生儿培养上清液中的干扰素-γ和IL-10水平相似，而HBeAg(+)新生儿在rHBcAg刺激下产生的肿瘤坏死因子-α高于HBeAg(-)新生儿。以上结果提示，母体环境对脐血T细胞表型无明显影响，但可促进新生儿非特异性Th1型细胞因子的产生。
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.