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在慢性乙型肝炎患者中,CTLA4调节B细胞受体信号,以抑制HBsAb分泌

Shengxia Yin¹, Minxin Mao², Linyan Gong²

¹Department of Infectious Diseases, Nanjing Drum Tower Hospital, Clinical College of Nanjing Medical University, Nanjing, Jiangsu, China; Institute of Viruses and Infectious Diseases, Nanjing University, Jiangsu, China.

Biochimica et biophysica acta. Molecular basis of disease

|April 25, 2025

概括

在B细胞上准CTLA4可能有助于治愈慢性乙肝病毒 (CHB) 感染. 我们的研究发现CTLA4损害了B细胞功能,其去除恢复了模型中的抗HBs抗体分泌和病毒清除.

科学领域:

免疫学免疫学免疫学
肝病学肝病学是一种肝病学.
病毒学病毒学

背景情况:

恢复B细胞功能是慢性乙型肝炎病毒 (CHB) 功能治愈的关键,但目标尚不清楚.
B细胞缺陷导致无法清除HBV感染.
细胞毒性T-淋巴细胞相关蛋白4 (CTLA4) 是B细胞恢复的潜在目标.

研究的目的:

研究CTLA4在B细胞功能障碍中的作用.
探索CTLA4作为治疗点,以实现CHB的功能治愈.
阐明CTLA4影响B细胞信号传递的机制.

主要方法:

从CHB患者的外周和肝脏B细胞中分析CTLA4表达.
单细胞RNA测序以评估记忆B细胞中的信号通路.
在体外实验中从B细胞中消耗CTLA4,在体内研究中使用HBV小鼠模型.

主要成果:

在CHB患者的HBsAg特异性B细胞中,CTLA4被上调; peginterferon-α治疗降低了CTLA4的表达.
CHB B细胞显示IL-6 JAK/STAT3和IL-2/STAT5信号减少,与抗体分泌受损相关.
在实验室中,CTLA4的减少恢复了HBsAb的分泌,并在HBV小鼠模型中改善了抗HBs幽默反应和病毒清除.
CTLA4直接结合SHP-1,损害了Jak-STAT和B细胞受体信号传递.

结论:

在CHB中,CTLA4在B细胞功能障碍中起着重要作用.
针对B细胞的CTLA4提供了一个有希望的策略来治疗CHB的功能性治疗.
了解CTLA4的机制为新的治疗干预提供了基础.

关键词:

抗HBss是什么意思细胞毒性T淋巴细胞相关的抗原-4 特定于HBsAg的B细胞.乙型肝炎病毒的感染.

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