Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1
Dysfunction and infection of freshly isolated blood myeloid and plasmacytoid dendritic cells in patients infected with HIV-1
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DOI：
10.1182/blood-2002-10-3189
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发表时间：
2003-06-01
期刊：
影响因子：
20.3
通讯作者：
Patterson, S
中科院分区：
文献类型：
--
作者：
Donaghy, H;Gazzard, B;Patterson, S
最近的研究表明，在HIV-1感染中，两类树突状细胞(DC)减少，分别称为浆细胞样树突状细胞(PcDCs)和髓系树突状细胞(MyDCs)。这项研究旨在确定这些人群是否是HIV-1感染的目标，以及他们刺激T淋巴细胞增殖的能力是否受到影响。从未接受抗逆转录病毒治疗的患者的血液中分离高纯度的myDC和pcDC，并通过聚合酶链式反应(PCR)评估HIV前病毒的水平。我们表明，这两个群体都是HIV-1感染的目标，正如14个PCDC中12个和14个MyDC样本中13个样本中存在前病毒所表明的那样。这种前病毒的一部分整合在myDC中。来自HIV-1感染者的myDC和pcDC在6天的混合白细胞反应中刺激同种异体T淋巴细胞增殖的能力严重受损，但不是由T淋巴细胞的继发感染介导的。因此，除了耗竭外，髓系和浆细胞样树突状细胞都会受到感染，并表现出功能受损。这些发现表明，树突状细胞的感染、耗尽和功能障碍可能是与HIV-1疾病相关的免疫抑制的原因之一。(C)2003年，由美国血液病学会提供。
Recently it has been shown that the 2 populations of blood dendritic cells (DCs), termed plasmacytoid (pcDCs) and myeloid (myDCs), are reduced in HIV-1 infection. This study aimed to deter mine whether these populations are targets for HIV-1 infection and whether their ability to stimulate T-lymphocyte proliferation is affected. Highly purified populations of myDCs and pcDCs were isolated from the blood of antiretroviral treatment-naive patients and assessed for the level of HIV provirus by polymerase chain reaction (PCR). We show that both populations are targets for HIV-1 infection as indicated by the presence of provirus in 12 of 14 pcDC and 13 of 14 myDC samples tested. A proportion of this provirus is integrated in myDCs. The ability of both myDCs and pcDCs from HIV-1-infected patients to stimulate allogeneic T-lymphocyte proliferation in a 6-day mixed leukocyte reaction was severely impaired, but was not mediated by secondary infection of T lymphocytes. Thus, in addition to depletion, both myeloid and plasmacytoid DCs are infected and show impaired functional capacity. These findings suggest that infection, depletion, and dysfunction of dendritic cells may contribute to the immunosuppression associated with HIV-1 disease. (C) 2003 by The American Society of Hematology.