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HIV介导的B淋巴细胞激活与淋巴瘤发生。

HIV-mediated B-lymphocyte activation and lymphomagenesis.

作者信息

Monroe J G, Silberstein L E

机构信息

Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia 19104, USA.

出版信息

J Clin Immunol. 1995 Mar;15(2):61-8. doi: 10.1007/BF01541733.

Abstract

Non-Hodgkin's (1ii)lymphoma is an AIDS-defining event in a significant percent of U.S. patients infected with the human immunodeficiency virus (HIV). Advances in anti-retroviral treatment and management of opportunistic infection have been accompanied by an increase in the incidence of these lymphomas. In the immunocompromised state of patients late in the course of HIV infection, these lymphomas represent a complication of HIV infection that is associated with an extremely poor prognosis. Currently, there is little understanding of the pathogenesis of HIV-associated lymphomas, which are nearly exclusively of B-cell origin. Experimental data do not support HIV infection in these lymphomas. While some lymphomas show evidence of EBV infection, the majority do not. Polyclonal B-cell hyperactivity during the early phases of HIV infection argues that chronic B-cell stimulation may be the major process predisposing B-cells in the HIV-infected individual to malignant transformation. The mechanism of this stimulation of normal B cells and its relationship to AIDS-associated lymphomas remain poorly understood. In this review, we will summarize current information on HIV-associated B lymphoma and then discuss our views on the association and regulation of HIV-related hyperactivity on the pathogenesis of this lymphoma.

摘要

在相当比例的美国感染人类免疫缺陷病毒(HIV)的患者中,非霍奇金淋巴瘤是艾滋病的定义性疾病。抗逆转录病毒治疗和机会性感染管理的进展伴随着这些淋巴瘤发病率的上升。在HIV感染后期患者的免疫功能低下状态下,这些淋巴瘤是HIV感染的一种并发症,预后极差。目前,对HIV相关淋巴瘤的发病机制了解甚少,这些淋巴瘤几乎均起源于B细胞。实验数据不支持这些淋巴瘤中的HIV感染。虽然一些淋巴瘤显示出EBV感染的证据,但大多数并非如此。HIV感染早期的多克隆B细胞过度活跃表明,慢性B细胞刺激可能是使HIV感染个体中的B细胞易于发生恶性转化的主要过程。这种对正常B细胞的刺激机制及其与艾滋病相关淋巴瘤的关系仍知之甚少。在本综述中,我们将总结关于HIV相关B淋巴瘤的当前信息,然后讨论我们对HIV相关过度活跃与该淋巴瘤发病机制之间关联及调控的看法。

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