摘要
目的研究3种人类白细胞抗G(humanleukocyteantigenG,HLA-G)受体CD158d(KIR2DL4)、CD85(jILT-2)和CD85d(ILT-4)在原发性胆汁性肝硬化(primarybiliarycirrhosis,PBC)患者外周血自然杀伤细胞(naturalkillercell,NK细胞)、CD4+T淋巴细胞和B细胞的表达情况,分析患者的主要淋巴细胞亚群是否存在HLA-G调节通路的缺陷。方法分离PBC患者和健康对照者外周血单个核细胞,利用免疫磁珠激活CD4+T淋巴细胞,利用流式细胞术分析NK细胞、CD4+T淋巴细胞和B细胞表面3种HLA-G受体的表达情况。结果患者NK细胞表面CD158d、CD85j的表达和CD4+T淋巴细胞表面CD158d的表达均较健康对照者明显下降。结论 PBC患者免疫效应细胞存在HLA-G受体表达的下调现象,提示HLA-G通路在PBC中存在异常,并很可能参与PBC的发病和进展。
Objective To investigate the expressions of human leukocyte antigen （HLA）-G receptors, CD158d（KIR2DIA）, CD85j （ILT-2） and CD85d （ILT-4） on natural killer （NK） cells, CD4＋ T cells and B cells from peripheral blood of patients with primary biliary cirrhosis （PBC）, and analyze whether HLA-G-based immunoregulation pathways of main lymphocyte subsets are impaired or not. Methods Peripheral blood mononuclear cells from PBC patients and healthy controls were isolated. CD4＋ T cells were stimulated by immunobeads; the expressions of 3 kinds of HLA-G receptors on NK cells, CD4＋ T cells and B cells were analyzed by flow cytometry. Results Compared to healthy controls, the expressions of HLA-G receptors CDlJ8d and CD85j on NK cells and CD158d on CD4＋ T cells from PBC patients significantly decreased with or without activation. Conclusions The expressions of HLA-G receptors on immune effector cells from PBC patients are down-regulated, indicating that HLA-G-based immunoregulation pathway is impaired in PBC patients, and the HLA-G molecules may thus contribute to the pathogenesis and progression of PBC.
出处
《传染病信息》
2011年第5期275-278,共4页
Infectious Disease Information
关键词
肝硬化
胆汁性
HLA抗原
liver cirrhosis, biliary
HLA antigens
