Increase of C1q biosynthesis in brain microglia and macrophages during lentivirus infection in the rhesus macaque is sensitive to antiretroviral treatment with 6-chloro-2',3'-dideoxyguanosine
Increase of C1q biosynthesis in brain microglia and macrophages during lentivirus infection in the rhesus macaque is sensitive to antiretroviral treatment with 6-chloro-2',3'-dideoxyguanosine
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DOI：
10.1016/j.nbd.2005.01.030
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发表时间：
2005-10-01
影响因子：
6.1
通讯作者：
Weihe, E
中科院分区：
文献类型：
--
作者：
Depboylu, C;Schäfer, MKH;Weihe, E
大脑中的补体激活有助于神经炎性和神经退行性疾病的病理，如神经艾滋病。应用半定量原位杂交和免疫组织化学方法，观察到猴免疫缺陷病毒(SIV)感染猕猴时，C1q在中枢神经系统中的表达早期持续增加。小胶质/巨噬细胞系的细胞是C1q蛋白和转录本的来源。在SIV脑炎脑组织中，C1q表达于增殖细胞和浸润性细胞中。所有SIV阳性细胞也均为C1q阳性。中枢神经系统特指的抗逆转录病毒药物6-氯-2‘，3’-二脱氧鸟苷治疗减少了C1q的合成，以及SIV负担和局部炎症反应在有艾滋病症状的猴子的大脑中。因此，先天免疫的经典补体臂的激活是神经艾滋病的早期事件，可能是干预的目标。(C)2005 Elsevier Inc.保留所有权利。
Complement activation in the brain contributes to the pathology of neuroinflammatory and neurodegenerative diseases such as neuro-AIDS. Using semiquantitative in situ hybridization and immunohistochemistry, we observed an early and sustained increase in the expression of C1q, the initial recognition subcomponent of the classical complement cascade, in the CNS during simian immunodeficiency virus (SIV) infection of rhesus macaques. Cells of the microglial/ macrophage lineage were the sources for C1q protein and transcripts. C1q expression was observed in proliferating and infiltrating cells in SIV-encephalitic brains. All SIV-positive cells were also C1q-positive. Treatment with the CNS-permeant antiretroviral agent 6-chloro-2',3'- dideoxyguanosine decreased C1q synthesis along with SIV burden and focal inflammatory reactions in the brains of AIDS-symptomatic monkeys. Thus, activation of the classical complement arm of innate immunity is an early event in neuro-AIDS and a possible target for intervention. (c) 2005 Elsevier Inc. All rights reserved.