Treatment of chronic hepatitis B with pegylated-interferon-α-2a (PegIFNα) in pediatric patients can lead to a higher rate of hepatitis B virus (HBV) surface antigen (HBsAg) loss than in adults. However, the mechanism of underlying immune response is not clear. The aim of this study was to explore innate and adaptive immunity, especially HBV-specific T cell responses in hepatitis B e antigen (HBeAg)-positive pediatric patients, who have experienced HBsAg loss. Isolated lymphocytes of 20 HBeAg-positive pediatric patients were collected every 12 weeks until treatment was stopped. The phenotype of T/natural killer (NK) cells and function of HBV-specific T cells were analyzed by flow cytometry. The frequency of CD69 and tumor necrosis factor-related apoptosis-inducing ligand (TRAIL) expressed on T cells and TRAIL on CD56hi NK cells in patients with HBsAg loss was remarkably higher compared with nonresponse patients. Furthermore, in vitro peptide stimulation of HBV-specific T cell responses was increased in patients with HBsAg loss when compared with week 0 and 48, and correlated with decline of viral load. The PegIFNα therapy in pediatric patients triggered T/NK cell activation and HBV-specific T cell responses, thereby contributing to successful viral control.

中文翻译：

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聚乙二醇干扰素-α-2a治疗乙型肝炎e抗原阳性小儿患者后，可增强乙肝病毒特异性T细胞应答。

与成人相比，在儿童患者中使用聚乙二醇化干扰素-α-2a（PegIFNα）治疗慢性乙型肝炎可导致乙型肝炎病毒（HBV）表面抗原（HBsAg）损失的发生率更高。但是，潜在的免疫反应机制尚不清楚。这项研究的目的是探讨先天性和适应性免疫，特别是在经历了HBsAg丢失的乙型肝炎e抗原（HBeAg）阳性儿童患者中的HBV特异性T细胞反应。每12周收集20例HBeAg阳性小儿患者的分离的淋巴细胞，直到停止治疗为止。通过流式细胞仪分析T /自然杀伤（NK）细胞的表型和HBV特异性T细胞的功能。HBsAg丢失患者的CD69和肿瘤坏死因子相关的凋亡诱导配体（TRAIL）在T细胞上表达的频率以及CD56hi NK细胞上TRAIL的表达频率显着高于无反应的患者。此外，与第0周和第48周相比，HBsAg丢失的患者对HBV特异性T细胞应答的体外肽刺激增加，并且与病毒载量下降相关。儿科患者中的PegIFNα治疗触发了T / NK细胞活化和HBV特异性T细胞应答，从而有助于成功地控制病毒。