HBV宫内感染新生儿外周血调节性T细胞表达

Detection and analysis of CD4^+CD25^+ regulatory T cell in peripheral blood from newborns with HBV intrauterine infection

目的探讨CD4+CD25+调节性T细胞(Treg)在乙肝病毒(HBV)宫内感染新生儿外周血中的表达和意义。方法选择乙肝表面抗原(HBsAg)阳性孕妇及其分娩新生儿79例,用酶联免疫吸附试验检测孕妇和新生儿外周血HBV标志物,实时荧光定量PCR检测母亲和新生儿外周血HBV DNA含量,用流式细胞仪检测新生儿外周血CD4+CD25+Treg和CD4+CD25+Foxp3+Treg水平。结果宫内感染HBV新生儿外周血CD4+CD25+Treg和CD4+CD25+Foxp3+Treg占CD4+T细胞比例分别为(10.57±2.25)%和(1.67±0.37)%,均高于未感染新生儿,差异有统计学意义(P<0.05),随产妇HBV DNA载量增加,新生儿外周血CD4+CD25+Treg和CD4+CD25+Foxp3+Treg增加,CD4+CD25+Treg比例高于阴性组(P<0.05);CD4+CD25+Treg和CD4+CD25+Foxp3+Treg均与产妇HBV DNA载量呈正相关(r=0.430、0.409,P<0.05)。结论 Treg可能通过抑制机体细胞免疫反应影响乙肝病毒清除,新生儿HBV宫内感染可能与Treg表达上调有关。

Objective To investigate the expression and significance of CD4^＋ CD25^＋ regulatory T cells in periph- eral blood from newborns with hepatitis B virus（HBV） intrauterine infection. Methods We selected 79 hepatitis B virus surface antigen（HBsAg） positive pregant women and their newborns. The HBV markers of the pregnant women and the neonates were detected with enzyme-linked immunosorbant assay （ELISA）. HBV DNA contents of pregnant women and neonates were detected with real-time fluorescent quantitative-PCR（RT-PCR）. The expression of CD4 ^＋ CD25 ＋ regulatory T cells（Tregs） in peripheral blood from the newborns were detected and analyzed with flow cytometer. Results The per- centage of CD4^＋ CD25^＋ Tregs/CD4^＋ and CD4^＋ CD25^＋ Foxp3^＋ Tregs/CD4^＋ were 10.57±2.25% and 1.67±0.37% in peripheral blood from the newborns of intrauterine infection group and were significantly higher than those of non-intrauterine infection group （P〈 0.05）. The expression of CD4^＋ CD25^＋ Tregs and CD4^＋ CD25^＋ Foxp3^＋ Tregs increased with maternal blood HBV DNA level. The proportion of CD4^＋ CD25^＋ Tregs was significantly higher than that of nega- tive group（ P〈0.05）. The expression of CD4^＋ CD25^＋ Tregs and CD4^＋ CD25^＋ Foxp3^＋ Tregs were correlated positively with HBV DNA level in pregnant mothers （r =0.430, r=0.409, P〈0.05 ）. Conclusion CD4^＋ CD25^＋ regulatory T cells could inhibit the elimination of HBV through suppressing cellular immune response, and its upregulation of expres- sion may be responsible for HBV inntrauterine infection.