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热带痉挛性截瘫/人嗜T淋巴细胞病毒1型相关脊髓病(TSP/HAM)中RANTES和MIP-1α的高表达

High production of RANTES and MIP-1alpha in the tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM).

作者信息

Montanheiro Patricia, Vergara Maria Paulina Posada, Smid Jerusa, da Silva Duarte Alberto José, de Oliveira Augusto César Penalva, Casseb Jorge

机构信息

Department of Dermatology, Sao Paulo University Medical School, Sao Paulo, Sao Paulo, Brazil.

出版信息

J Neuroimmunol. 2007 Aug;188(1-2):138-42. doi: 10.1016/j.jneuroim.2007.05.015. Epub 2007 Jun 22.

Abstract

Human T cell lymphotropic virus type 1 (HTLV-1) infection is associated with progressive neurological disorders and tropical spastic paraparesis/HTLV-1-associated myelopathy (TSP/HAM). The pathogenesis of TSP/HAM is considered as immune mediated, involving cytotoxic T cell (CTL) responses to a number of viral proteins and notably the regulation protein Tax. T CD8+ cells produce beta-chemokines, which are important in the anti-viral response. In the present study, we have analyzed the CC chemokines (RANTES, MIP-1beta and MIP-1alpha) production in retrovirus-infected subjects. A total of 191 subjects were studied: 52 healthy controls, 72 asymptomatic HTLV-1-infected carriers and 67 TSP/HAM patients. Peripheral blood mononuclear cells were maintained in the presence or absence of PHA, and supernatant fluids were assayed using EIA. MIP-1beta concentration was not significantly different across groups, but RANTES and MIP-1alpha concentrations showed significant differences when the three groups were compared. In TSP/HAM patients, the increase in the production of chemokines may lead to a recruitment of pro-inflammatory factors, contributing to the membrane's myelin damage.

摘要

人类嗜T细胞病毒1型(HTLV-1)感染与进行性神经疾病及热带痉挛性截瘫/HTLV-1相关脊髓病(TSP/HAM)有关。TSP/HAM的发病机制被认为是免疫介导的,涉及细胞毒性T细胞(CTL)对多种病毒蛋白尤其是调节蛋白Tax的反应。T CD8+细胞产生β趋化因子,其在抗病毒反应中很重要。在本研究中,我们分析了逆转录病毒感染受试者中CC趋化因子(RANTES、MIP-1β和MIP-1α)的产生情况。共研究了191名受试者:52名健康对照者、72名无症状HTLV-1感染携带者和67名TSP/HAM患者。外周血单个核细胞在有或无PHA的情况下培养,上清液用酶免疫测定法检测。各组间MIP-1β浓度无显著差异,但比较三组时RANTES和MIP-1α浓度显示出显著差异。在TSP/HAM患者中,趋化因子产生的增加可能导致促炎因子的募集,从而导致髓鞘膜损伤。

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