Gazouli Maria, Zavos George, Papaconstantinou Ioannis, Lukas John C, Zografidis Anastassios, Boletis John, Kostakis Alkiviadis
Department of Histology-Embryology, Medical School, University of Athens, Athens, Greece.
Anticancer Res. 2004 Mar-Apr;24(2C):1311-4.
Kaposi's sarcoma (KS), an angio-proliferative inflammation lesion, is frequently secondary to clinical immunosuppression such as after renal transplantation. KS growth is promoted by the inflammatory cytokine interleukin-6 (IL-6) and is also correlated with human herpesvirus-8 (HHV-8) infection.
In a sample of 15 renal transplant patients with KS and 40 patients without KS, we explored the influence of genetic differences in the production of IL-6 by promoter polymorphisms G-174C as well as the correlation with HHV-8 DNA.
The G allele homozygotes, which are associated with increased IL-6 production, had increased KS incidence (p=0.008). Therefore increased IL-6 production constitutes a risk factor which should be considered in clinical immunosuppression.
In addition to the HHV-8 infection, the interleukin-6 promoter polymorphism G-174C is associated with a risk of development of KS in renal transplant recipients.
卡波西肉瘤(KS)是一种血管增殖性炎症病变,常继发于临床免疫抑制状态,如肾移植后。KS的生长由炎性细胞因子白细胞介素-6(IL-6)促进,并且也与人疱疹病毒8型(HHV-8)感染相关。
在15例患有KS的肾移植患者和40例无KS的患者样本中,我们探究了启动子多态性G-174C在IL-6产生中的基因差异影响以及与HHV-8 DNA的相关性。
与IL-6产生增加相关的G等位基因纯合子,其KS发病率增加(p = 0.008)。因此,IL-6产生增加构成了一个危险因素,在临床免疫抑制中应予以考虑。
除HHV-8感染外,白细胞介素-6启动子多态性G-174C与肾移植受者发生KS的风险相关。