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白细胞介素-18血清水平升高与疾病进展相关,且可能导致HIV-1感染患者的病毒学治疗失败。

Raised serum levels of interleukin-18 is associated with disease progression and may contribute to virological treatment failure in HIV-1-infected patients.

作者信息

Stylianou E, Bjerkeli V, Yndestad A, Heggelund L, Waehre T, Damås J K, Aukrust P, Frøland S S

机构信息

Section of Clinical Immunology and Infectious Diseases, Rikshospitalet University Hospital, Oslo, Norway.

出版信息

Clin Exp Immunol. 2003 Jun;132(3):462-6. doi: 10.1046/j.1365-2249.2003.02179.x.

Abstract

To gain further insight into the possible role of interleukin (IL)-18 in HIV-1 infection we examined serum levels of IL-18 in various clinical and immunological stages of HIV-1 infection during cross-sectional (n = 41) and longitudinal testing (n = 20) and during HAART (n = 21, 24 months follow-up). Our main findings were that HIV-1-infected patients had significantly raised IL-18 levels comparing healthy controls, particularly in those with advanced disease, that while HAART induced a marked decline in IL-18, virological treatment failure was associated with persistently raised IL-18 levels during such therapy and that our in vitro experiments showed an IL-18-mediated up-regulation of the HIV-1 coreceptor CXCR4 and the pro-apoptotic mediator TRAIL in PBMC from HIV-1-infected patients receiving HAART. HIV-1 infection appears to be characterized by persistently raised IL-18 levels and during HAART, such a pattern was associated with virological treatment failure, possibly contributing to immunodeficiency and HIV-1 replication in these patients.

摘要

为了进一步深入了解白细胞介素(IL)-18在HIV-1感染中可能发挥的作用,我们在横断面研究(n = 41)、纵向检测(n = 20)以及高效抗逆转录病毒治疗(HAART,n = 21,随访24个月)期间,检测了处于HIV-1感染不同临床和免疫阶段患者的血清IL-18水平。我们的主要发现包括:与健康对照相比,HIV-1感染患者的IL-18水平显著升高,尤其是在疾病晚期患者中;虽然HAART使IL-18水平显著下降,但病毒学治疗失败与治疗期间IL-18水平持续升高有关;我们的体外实验表明,IL-18可介导接受HAART的HIV-1感染患者外周血单核细胞(PBMC)中HIV-1共受体CXCR4和促凋亡介质TRAIL的上调。HIV-1感染似乎以IL-18水平持续升高为特征,在HAART期间,这种模式与病毒学治疗失败有关,可能导致这些患者的免疫缺陷和HIV-1复制。

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Interleukin-18 regulates both Th1 and Th2 responses.白细胞介素-18调节Th1和Th2反应。
Annu Rev Immunol. 2001;19:423-74. doi: 10.1146/annurev.immunol.19.1.423.

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