Kannagi M, Chalifoux L V, Lord C I, Letvin N L
Harvard Medical School, New England Regional Primate Research Center, Southborough, MA 01772.
J Immunol. 1988 Apr 1;140(7):2237-42.
The AIDS-like disease in rhesus monkeys induced by the simian immunodeficiency virus (SIV) has been used as a model to explore the nature of the T lymphocyte response after infection with viruses of the human immunodeficiency virus family. Activated CD8+ lymphocytes are present in increased numbers in the paracortex of lymph nodes of SIV-infected rhesus monkeys with a lymphadenopathy syndrome. We demonstrate that SIV is more readily isolated from CD8+ lymphocyte-depleted PBL of SIV-infected animals than from their unfractionated PBL. Rather than reflecting the fact that the CD8+ lymphocyte-depleted cell populations are simply enriched for CD4+ lymphocytes, this indicates that CD8+ cells themselves are critical in this regulatory interaction. In fact, CD8+ lymphocytes from SIV-infected but not uninfected rhesus monkeys can block SIV replication in vitro in PBL populations. A T lymphocyte population that blocks replication of viruses of the HIV family may contribute to containing the progression of AIDS.
由猴免疫缺陷病毒（SIV）诱发的恒河猴类艾滋病疾病已被用作一种模型，以探究感染人类免疫缺陷病毒家族病毒后T淋巴细胞反应的本质。在患有淋巴结病综合征的SIV感染恒河猴的淋巴结副皮质中，活化的CD8 +淋巴细胞数量增加。我们证明，与未分级的外周血淋巴细胞（PBL）相比，从SIV感染动物的CD8 +淋巴细胞耗竭的PBL中更容易分离出SIV。这并非反映CD8 +淋巴细胞耗竭的细胞群体只是富含CD4 +淋巴细胞这一事实，而是表明CD8 +细胞本身在这种调节相互作用中至关重要。事实上，来自SIV感染而非未感染的恒河猴的CD8 +淋巴细胞可在体外阻断PBL群体中的SIV复制。一个能阻断HIV家族病毒复制的T淋巴细胞群体可能有助于遏制艾滋病的进展。
