Jin Xin, Yan Zhi-Han, Lu Lingna, Lu Shengjia, Zhang Guoping, Lin Wei
Department of Clinical Laboratory, Tongde Hospital of Zhejiang Province, Hangzhou, China.
Department of Hepatology, Wuxi Fifth People's Hospital, Wuxi, China.
Front Med (Lausanne). 2021 Oct 26;8:759292. doi: 10.3389/fmed.2021.759292. eCollection 2021.
After infection of hepatitis B virus (HBV), the virus induces a variety of immune disorders in the host, leading to immune escape and, finally, the chronicity of the disease. This study investigated immune cell defects and functional impairment in patients with chronic hepatitis B (CHB). We analyzed the percentage, function, and phenotypes of various immune cell subpopulations in the peripheral blood along with the concentrations of cytokines in the plasma. We compared the results between patients with CHB and healthy individuals. It was found that in patients with CHB, the cell function was impaired and, there was increased expression of inhibitory receptors, such as NKG2A and PD-1 in both NK and T cells. The impairment of function was mainly in cytokine secretion, and the cytotoxicity was not significantly diminished. We also found that the proportion of dendritic cells (DC) decreased and regulatory B cells (Breg) increased in CHB. In addition, the Breg cells were negatively correlated with T cell cytokine and positively correlated with ALT and HBV viral load. Taken together, various disorders and functional impairments were found in the immune cells of peripheral blood in CHB patients, especially NK and T cells. These cells showed exhaustion and the increase of regulatory B cells may be one of the reasons for this phenomenon.
感染乙型肝炎病毒(HBV)后,该病毒会在宿主体内引发多种免疫紊乱,导致免疫逃逸,最终致使疾病慢性化。本研究调查了慢性乙型肝炎(CHB)患者的免疫细胞缺陷和功能损害情况。我们分析了外周血中各种免疫细胞亚群的百分比、功能和表型,以及血浆中细胞因子的浓度。我们比较了CHB患者和健康个体之间的结果。结果发现,在CHB患者中,细胞功能受损,NK细胞和T细胞中抑制性受体如NKG2A和PD-1的表达增加。功能损害主要在于细胞因子分泌,细胞毒性并未显著降低。我们还发现,CHB患者中树突状细胞(DC)比例下降,调节性B细胞(Breg)增加。此外,Breg细胞与T细胞细胞因子呈负相关,与ALT和HBV病毒载量呈正相关。综上所述,CHB患者外周血免疫细胞存在多种紊乱和功能损害,尤其是NK细胞和T细胞。这些细胞表现出耗竭,调节性B细胞的增加可能是导致这种现象的原因之一。