HIV和SIV感染中滤泡树突状细胞-B细胞相互作用增强及其在多克隆B细胞激活中的潜在作用。

Y J Rosenberg, M G Lewis, M H Kosco-Vilbois
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引用次数: 10

摘要

人类免疫缺陷病毒(HIV)感染的特征一方面是多克隆b细胞激活和对b细胞生长因子的反应增强,另一方面是特异性抗体(Ab)反应的丧失和对b细胞激活的正常信号的难反应。HIV和猿猴免疫缺陷病毒(SIV)感染者淋巴结的组织病理学研究表明,最初的滤泡增生和大的不规则生发中心的出现,伴随着滤泡树突状细胞(FDC)的破坏而逐渐退化。在这一过程中,与未感染的对照组相比,滤泡树突状细胞富集的淋巴结细胞培养物表现出更强的诱导簇形成(“体外生发中心”)、淋巴细胞增殖和抗体产生的能力。本文讨论了在siv感染的生发中心内,fdc -B细胞相互作用增强可能导致选择高亲和力B细胞的能力降低,并改变抗体产生细胞和记忆细胞生成的动力学,从而导致观察到的过度活跃。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Enhanced follicular dendritic cell-B cell interaction in HIV and SIV infections and its potential role in polyclonal B cell activation.

Human immunodeficiency virus (HIV) infections have been characterized by both polyclonal B-cell activation and enhanced responsiveness to B-cell growth factors on one hand and the loss of specific antibody (Ab) responses and refractoriness to the normal signals for B-cell activation on the other. Histopathological studies of lymph node from HIV- and simian immunodeficiency virus (SIV)-infected individuals have indicated initial follicular hyperplasia and the appearance of large irregular germinal centers that undergo progressive involution concomitant with follicular dendritic-cell (FDC) disruption. During this process, follicular dendritic-cell-enriched lymph-node-cell cultures exhibit increased ability to induce cluster formation ("in vitro germinal centers"), lymphocyte proliferation and antibody production compared to uninfected controls. This paper discusses how enhanced FDC-B-cell interaction within SIV-infected germinal centers may result in a reduced ability to select high-affinity B cells and alter the dynamics of antibody-producing-cell and memory-cell generation resulting in the observed hyperactivity.

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