Hepatitis B core antigen stimulates interleukin-10 secretion by both T cells and monocytes from peripheral blood of patients with chronic hepatitis B virus infection
Hepatitis B core antigen stimulates interleukin-10 secretion by both T cells and monocytes from peripheral blood of patients with chronic hepatitis B virus infection
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DOI：
10.1111/j.1365-2249.2003.02376.x
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发表时间：
2004-03-01
影响因子：
4.6
通讯作者：
Imawari, M
中科院分区：
文献类型：
--
作者：
Hyodo, N;Nakamura, I;Imawari, M
在慢性乙型肝炎病毒（HBV）感染中，对乙型肝炎核心抗原（HBcAg）的免疫反应较弱。白细胞介素 (IL)-10 是一种有效的免疫抑制细胞因子，我们最近报道，慢性 HBV 感染患者或健康对照者的外周血单核细胞 (PBMC) 响应 HBcAg 分泌该细胞因子。使用酶联免疫斑点测定，我们比较了 16 名慢性 HBV 感染患者和 6 名健康对照者中 HBcAg 刺激 PBMC 产生 IL-10 的能力与脂多糖 (LPS)、植物血凝素-P 和丙型肝炎病毒衍生抗原的能力。在慢性 HBV 感染患者中，对 HBcAg 产生反应的 IL-10 斑点形成细胞 (SFC) 频率与用 LPS 获得的频率相当。慢性 HBV 感染患者中 IL-10 SFC 对 HBcAg 或 LPS 反应的频率显着高于健康对照。慢性 HBV 感染患者对 HBcAg 反应的 IL-10 SFC 由 26-35% T 细胞、62-70% 单核细胞和不到 1% B 细胞组成。在对照中，只有单核细胞参与 IL-10 的产生。血清丙氨酸转氨酶 (ALT) 升高且可检测到 HBV DNA 的患者中 HBcAg 刺激的 IL-10 SFC（代表 T 细胞和单核细胞）的频率显着高于 ALT 正常且 HBV DNA 检测不到的患者。 HBcAg 刺激 PBMC 产生 IL-10 的强大能力可能对 HBV 的免疫耐受有重要贡献。
In chronic hepatitis B virus (HBV) infection, immune responses to hepatitis B core antigen (HBcAg) are weak. Interleukin (IL)-10 is a potent immunosuppressive cytokine which we reported recently to be secreted in response to HBcAg by peripheral blood mononuclear cells (PBMCs) from patients with chronic HBV infection or healthy controls. Using an enzyme-linked immunospot assay, we compared the ability of HBcAg to stimulate IL-10 production by PBMC with that of lipopolysaccharide (LPS), phytohaemagglutinin-P and hepatitis C virus-derived antigens in 16 patients with chronic HBV infection and six healthy controls. Frequencies of IL-10 spot-forming cells (SFC) in response to HBcAg were comparable to those obtained with LPS in patients with chronic HBV infection. Frequencies of IL-10 SFC in response to HBcAg or to LPS were significantly higher in patients with chronic HBV infection than in healthy controls. IL-10 SFC in response to HBcAg consisted of 26-35% T cells, 62-70% monocytes and less than 1% B cells in patients with chronic HBV infection. Only monocytes contributed to IL-10 production in controls. Frequencies of HBcAg stimulated IL-10 SFC representing T cells and monocytes were significantly higher in patients with elevated serum alanine aminotransferase (ALT) and detectable HBV DNA than in patients with normal ALT and undetectable HBV DNA. The potent ability of HBcAg to stimulate IL-10 production by PBMC may contribute importantly to immune tolerance toward HBV.