期刊
AMERICAN JOURNAL OF PATHOLOGY
卷 164, 期 5, 页码 1557-1566出版社
ELSEVIER SCIENCE INC
DOI: 10.1016/S0002-9440(10)63714-5
关键词
-
类别
资金
- NCRR NIH HHS [P20 RR016443, RR-16443] Funding Source: Medline
- NIAID NIH HHS [AI-29382] Funding Source: Medline
- NIMH NIH HHS [MH-62969-01, MH068212, R01 MH068212] Funding Source: Medline
- NINDS NIH HHS [NS-32203] Funding Source: Medline
Inflammatory mediators play a crucial role in the pathophysiology of several neurodegenerative diseases including acquired immune deficiency syndrome dementia complex. In the present study we identified a link between CXCL10 overexpression in the brain and human immunodeficiency virus dementia and demonstrated the presence of the chemokine CXCL10 and its receptor, CXCR3, in the neurons in the brains of macaques with simian human immunodeficiency virus encephalitis. Using human fetal brain cultures, we showed that treatment of these cells with either SHIV89.6P or viral gp120 resulted in induction of CXCL10 in neurons. Cultured neurons treated with the chemokine developed increased membrane permeability followed by apoptosis via activation of caspase-3. We confirmed the relevance of these findings in sections of human and macaque brains with encephalopathy demonstrating that neurons expressing CXCL10 also expressed caspase-3.
作者
我是这篇论文的作者
点击您的名字以认领此论文并将其添加到您的个人资料中。
推荐
暂无数据