HIV INDUCES THYMUS DEPLETION INVIVO
HIV INDUCES THYMUS DEPLETION INVIVO
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DOI：
10.1038/363728a0
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发表时间：
1993-06-24
期刊：
影响因子：
64.8
通讯作者：
KANESHIMA, H
中科院分区：
文献类型：
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作者：
BONYHADI, ML;RABIN, L;KANESHIMA, H
人类免疫缺陷病毒（HIV）疾病的典型特征是外周循环中的CD 4 + T淋巴细胞计数下降，这种损失可能继发于加速破坏、抑制分化和/或将循环细胞隔离到组织间隙中。由于在人类受试者中很难区分这些可能性，因此与HIV感染相关的致病机制尚不清楚。特别是，很少有人知道的事件发生在受感染的淋巴器官，其中大多数CD 4 T淋巴细胞成熟和功能1，2。为了更好地描述体内HIV发病机制，我们将人血淋巴样器官植入免疫缺陷的SCID小鼠中，以产生SCID-hu小鼠3，4。我们以前已经表明，这些器官系统促进长期多谱系人类造血，并允许感染艾滋病毒5，6。在这里，我们报告说，人类胸腺细胞生成抑制艾滋病毒感染，从而排除再生的外周T细胞室。
HUMAN immunodeficiency virus (HIV) disease is typified by declining CD4+ T lymphocyte counts in the peripheral circulation, a loss which may be secondary to accelerated destruction, to suppressed differentiation, and/or to sequestration of circulating cells into tissue spaces. As it is hard to distinguish between these possibilities in human subjects, the pathogenic mechanisms associated with HIV infection are unclear. In particular, little is known about the events that occur within infected lymphoid organs in which most CD4 T lymphocytes mature and function1,2. To obtain a better description of HIV pathogenesis in vivo, we have implanted human haematolymphoid organs into the immunodeficient SCID mouse to create the SCID-hu mouse3,4. We have previously shown that these organ systems promote long-term multilineage human haematopoiesis and are permissive for infection with HIV5,6. Here we report that human thymopoiesis is suppressed by HIV infection, thereby precluding regeneration of the peripheral T-cell compartment.