Dysfunctional Epstein-Barr virus (EBV)-specific CD8(+) T lymphocytes and increased EBV load in HIV-1 infected individuals progressing to AIDS-related non-Hodgkin lymphoma.
Dysfunctional Epstein-Barr virus (EBV)-specific CD8(+) T lymphocytes and increased EBV load in HIV-1 infected individuals progressing to AIDS-related non-Hodgkin lymphoma.
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HIV-1 感染者进展为 AIDS 相关非霍奇金淋巴瘤时，EB 病毒 (EBV) 特异性 CD8(+) T 淋巴细胞功能失调，EBV 载量增加。
DOI：
10.1182/blood.v98.1.146
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发表时间：
2001
期刊：
影响因子：
20.3
通讯作者：
F. Miedema
中科院分区：
文献类型：
--
作者：
D. Baarle;E. Hovenkamp;M. Callan;K. Wolthers;S. Kostense;L. Tan;H. Niesters;A. Osterhaus;A. McMichael;M. Oers;F. Miedema
获得性免疫缺陷综合征相关的非霍奇金淋巴瘤（AIDS-NHL）被认为是由于EB病毒（EBV）特异性细胞免疫的丧失而产生的。在这里，进行了一项研究，以确定是否由于EBV特异性细胞毒性T细胞的物理损失或功能障碍而丧失了对EBV的细胞免疫。EBV特异性细胞免疫的数据与EBV载量相关。为了比较，研究了进展为艾滋病的机会性感染（AIDS-OI）和长期无症状（LTA）的个体。使用四聚体HLA-EBV-肽复合物检测病毒特异性T细胞的数量;使用干扰素-γ（IFN-γ）Elispot测定来确定这些EBV特异性T细胞的功能。观察到EBV特异性CD 8（+）T细胞在人类免疫缺陷病毒（HIV）感染个体中以正常数量存在。但与HIV（-）感染者相比，其功能能力有所下降。在AIDS-NHL患者中，EBV特异性T细胞在HIV-1感染过程中没有物理损失，但显示出其响应EBV肽产生IFN-γ的能力的进行性丧失。这种功能丧失与较低的CD 4（+）T细胞数量相关，并伴有EBV负荷增加。在HIV-1感染的LTA个体中，CD 4（+）T细胞数量保持不变，并进展为AIDS-OI，IFN-γ产生的EBV特异性T细胞稳定，EBV载量在HIV感染过程中保持稳定或下降，提示免疫控制。我们的数据表明，EBV特异性CD 8（+）T细胞的功能丧失伴随EBV负荷的增加可能在AIDS-NHL的发病机制中起作用。
Acquired immunodeficiency syndrome-related non-Hodgkin lymphomas (AIDS-NHL) are thought to arise because of loss of Epstein-Barr Virus (EBV)-specific cellular immunity. Here, an investigation was done to determine whether cellular immunity to EBV is lost because of physical loss or dysfunction of EBV-specific cytotoxic T cells. Data on EBV-specific cellular immunity were correlated with EBV load. For comparison, individuals who progressed to AIDS with opportunistic infections (AIDS-OI) and long-term asymptomatics (LTAs) were studied. The number of virus-specific T cells was detected using tetrameric HLA-EBV-peptide complexes; function of these EBV-specific T cells was determined using the interferon-gamma (IFN-gamma) Elispot assay. It was observed that EBV-specific CD8(+) T cells were present in normal numbers in human immunodeficiency virus (HIV)-infected individuals. However, their functional capacity was decreased compared with HIV(-) individuals. In AIDS-NHL patients, EBV-specific T cells were not physically lost in the course of HIV-1 infection but showed progressive loss of their capability to produce IFN-gamma in response to EBV peptides. This loss of function correlated with lower CD4(+) T-cell numbers and was accompanied by increasing EBV load. In HIV-1-infected LTA individuals, in whom CD4(+) T-cell numbers were maintained, and progressors to AIDS-OI, IFN-gamma-producing EBV-specific T cells were stable and EBV load remained stable or decreased in the course of HIV infection, suggestive of immune control. Our data indicate that functional loss of EBV-specific CD8(+) T cells with a concomitant increase in EBV load may play a role in the pathogenesis of AIDS-NHL.
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影响因子：
20.3
作者：
Rooney, CM;Smith, CA;Heslop, HE
通讯作者：
Heslop, HE
影响因子：
15.9
作者：
Speck, SH;Chatila, T;Flemington, E
通讯作者：
Flemington, E
影响因子：
56.9
作者：
Rosenberg, ES;Billingsley, JM;Walker, BD
通讯作者：
Walker, BD
DOI：
10.1093/infdis/155.5.877
发表时间：
1987-05
期刊：
The Journal of infectious diseases
影响因子：
--
作者：
R. Blumberg;T. Paradis;R. Byington;W. Henle;M. S. Hirscb;R. Schooley
通讯作者：
R. Blumberg;T. Paradis;R. Byington;W. Henle;M. S. Hirscb;R. Schooley
感染人类免疫缺陷病毒的患者发生与 Epstein-Barr 病毒相关的非霍奇金淋巴瘤。
影响因子：
20.3
作者：
Shibata,D;Weiss,LM;Hernandez,AM;Nathwani,BN;Bernstein,L;Levine,AM
通讯作者：
Levine,AM