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树突状细胞、调节性 T 细胞与慢性丙型肝炎的发病机制。

Dendritic cells, regulatory T cells and the pathogenesis of chronic hepatitis C.

机构信息

Department of Medicine, Rhode Island Hospital and the Warren Alpert Medical School at Brown University, Providence, RI, USA.

出版信息

Virulence. 2012 Nov 15;3(7):610-20. doi: 10.4161/viru.21823. Epub 2012 Oct 17.

Abstract

Hepatitis C virus (HCV) is a small, enveloped RNA virus and a major cause of chronic liver disease. Resolution of primary HCV infections depends upon the vigorous responses of CD4⁺ and CD8⁺ T cells to multiple viral epitopes. Although such broad-based responses are readily detected early during the course of infection regardless of clinical outcome, they are not maintained in individuals who develop chronic disease. Ostensibly, a variety of factors contribute to the diminished T cell responses observed in chronic, HCV-infected patients including impaired dendritic cell function and the induction of CD4⁺ FoxP3⁺ regulatory T cells. Overwhelming evidence suggests that the complex interaction of dendritic cells and regulatory T cells plays a critical role in the pathogenesis of chronic hepatitis C.

摘要

丙型肝炎病毒(HCV)是一种小型包膜 RNA 病毒,是慢性肝病的主要病因。原发性 HCV 感染的清除取决于 CD4+和 CD8+T 细胞对多种病毒表位的强烈反应。尽管无论临床结局如何,在感染过程的早期都能轻易地检测到这种广泛的反应,但在发展为慢性疾病的个体中却无法维持。表面上,多种因素导致慢性 HCV 感染患者的 T 细胞反应减弱,包括树突状细胞功能受损和 CD4+FoxP3+调节性 T 细胞的诱导。大量证据表明,树突状细胞和调节性 T 细胞的复杂相互作用在慢性丙型肝炎的发病机制中起着关键作用。

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