Differential susceptibility of peripheral blood CD5+ and CD5- B cells to apoptosis in chronic hepatitis C patients
Differential susceptibility of peripheral blood CD5+ and CD5- B cells to apoptosis in chronic hepatitis C patients
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DOI：
10.1016/j.bbrc.2009.09.012
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发表时间：
2009-11-20
影响因子：
3.1
通讯作者：
Yamaguchi, Kazunari
中科院分区：
文献类型：
--
作者：
Mizuochi, Toshiaki;Ito, Masahiko;Yamaguchi, Kazunari
大量证据表明，慢性丙型肝炎病毒（HCV）感染与B细胞异常之间存在密切联系，这些异常包括混合性冷球蛋白血症、类风湿因子（RF）产生以及可能发展为非霍奇金淋巴瘤的淋巴组织增生性疾病。最近的研究表明慢性丙型肝炎患者（CHC）外周血中CD 5（+）B细胞扩增。由于能够产生自身抗体和RE的CD 5（+）B细胞对于HCV相关发病机制的发展显然是至关重要的，因此慢性HCV感染后CD 5（+）和CD 5（-）B细胞亚群的命运是令人感兴趣的。在这项研究中，慢性HCV感染诱导每个B细胞亚群凋亡的程度进行了调查。结果表明CHC患者外周血CD 5（-）B细胞较CD 5（+）B细胞更易发生凋亡。此外，CHC中IL-4、IL-10和IL-12的血浆水平显著升高，从而表明这些白细胞介素保护CD 5（+）B细胞免于凋亡。不同的B细胞亚群在CHC的差异敏感性的基本原理也进行了讨论与慢性HCV感染相关的肝外表现。(C)2009爱思唯尔公司All rights reserved.
A body of evidence has Suggested a close link between chronic hepatitis C virus (HCV) infection and B cell abnomalities, including mixed cryoglobulinemia, rheumatoid factor (RF) production, and lymphoproliferative disorders that may develop into non-Hodgkin's lymphoma. Recent studies have demonstrated the expansion of CD5(+) B cells in the peripheral blood of chronic hepatitis C patients (CHC). As CD5(+) B cells, which are capable of producing autoantibodies and RE, are apparently crucial for the development of HCV-associated pathogenesis, the fate of both the CD5(+) and CD5(-) B cell subsets upon chronic HCV infection is of interest. In this study, the degree to which chronic HCV infection induces apoptosis in each B cell subset was investigated. Our results demonstrated that peripheral CD5(-) B cells were more susceptible to apoptosis than CD5(+) B cells in CHC. Furthermore, plasma levels of IL-4, IL-10, and IL-12 were significantly elevated in CHC, thus suggesting that these interleukins protect CD5(+) B cells from apoptosis. The rationale for the differential susceptibility of distinct B cell subsets in CHC is also discussed with regard to extrahepatic manifestations associated with chronic HCV infection. (C) 2009 Elsevier Inc. All rights reserved.