Decrease in hepatic CD56+ T cells and Vα24+ natural killer T cells in chronic hepatitis C viral infection

Decrease in hepatic CD56+ T cells and Vα24+ natural killer T cells in chronic hepatitis C viral infection
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DOI:
10.1016/s0168-8278(02)00072-7
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发表时间:
2002-07-01
影响因子:
25.7
通讯作者:
O'Farrelly, C
O'Farrelly, C
中科院分区:
医学1区
文献类型:
--
作者:
Deignan, T;Curry, MP;O'Farrelly, C

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背景/目的:肝内免疫系统可能在决定丙型肝炎病毒(HCV)感染的结果中发挥关键作用。肝淋巴细胞库的特点是高CD8/CD4 T细胞比率和大量的γ - δ T细胞、自然杀伤(NK)细胞、NK T细胞和NK受体阳性T细胞。目前尚不清楚这些人群中哪些对HCV免疫或免疫病理有贡献。方法:采用流式细胞术和免疫组织化学方法,比较了13例轻度慢性丙型肝炎感染患者、14例终末期丙型肝炎肝硬化患者和5例组织学正常肝脏的肝内淋巴细胞谱和细胞因子表达,探讨淋巴细胞亚群的相对贡献。结果:慢性HCV感染患者肝脏中携带TCR的CD4(+) T细胞显著扩增,CD56(+) T细胞和Valpha24 TCR阳性T细胞显著减少。扩增的CD4+T细胞主要是Th1细胞,产生干扰素- γ而不产生白细胞介素-4。结论:HCV感染的失败可能是由于先天和/或记忆免疫反应不足,而Th1细胞可能介导免疫病理。(C) 2002年欧洲肝脏研究协会。Elsevier Science B.V.版权所有。
Background/Aims: The intrahepatic immune system is likely to play a key role in determining the outcome of hepatitis C virus (HCV) infection. The hepatic lymphocyte repertoire is characterised by high CD8/CD4 T cell ratios and large numbers of gammadelta T cells, natural killer (NK) cells, NK T cells and NK receptor-positive T cells. It is not known which of these populations contribute to immunity against HCV or immune pathology.Methods: To explore the relative contributions of lymphocyte subpopulations, we have compared the intrahepatic lymphocyte repertoires and cytokine expression in 13 patients with mild chronic hepatitis C infection, 14 with end-stage hepatitis C cirrhosis and five histologically normal livers by flow cytometry and immunohistochemistry.Results: CD4(+) T cells bearing alphabeta T cell receptors (TCR) were significantly expanded in livers with chronic HCV infection while CD56(+) alphabeta T cells and Valpha24 TCR-positive T cells were significantly depleted. Expanded CD4+T cells were predominantly Th1 cells, producing interferon-gamma but not interleukin-4.Conclusions: Failure to resolve HCV infection may be due to deficient innate and/or memory immune responses, while Th1 cells may mediate immune pathology. (C) 2002 European Association for the Study of the Liver. Published by Elsevier Science B.V. All rights reserved.