期刊
NEUROCHEMISTRY INTERNATIONAL
卷 49, 期 2, 页码 145-153出版社
PERGAMON-ELSEVIER SCIENCE LTD
DOI: 10.1016/j.neuint.2006.04.002
关键词
multiple sclerosis; Alzheimer's disease; neurodegeneration; autoimmunity; EAE; facial axotomy; pattern recognition receptors; dendritic cells; antigen-presentation; antigen-presenting cell
资金
- NINDS NIH HHS [R01 NS039508-04, R01 NS045735-02, R01 NS039508-02, R01 NS045735-05, R01 NS045735-01, R01 NS039508-03, R01 NS045735, R01 NS039508, R01 NS039508-06, R01 NS039508-05, R01 NS045735-03, R01 NS039508-01A1S1, R01 NS045735-04, R01 NS039508-01A1] Funding Source: Medline
Microglial activation is one of the earliest and most prominent features of nearly all CNS neuropathologies often occurring prior to other indicators of overt neuropathology. Whether microglial activation in seemingly healthy CNS tissue during the early stages of several is a response to early stages of neuronal or glial distress or an early sign of microglial dysfunction causing subsequent neurodegeneration is unknown. Here we characterize and discuss how changes in the CNS microenvironment (neuronal activity/viability, glial activation) lead to specific forms of microglial activation. Specifically, we examine the potential role that TREM-2 expressing microglia may play in regulating the effector function of autoreactive T cell responses. Thus, we suggest that ubiquitous suppression of microglial activation during CNS inflammatory disorders rather than targeted manipulation of microglial activation, may in the end be maladaptive leading to incomplete remission of symptoms. (c) 2006 Published by Elsevier Ltd.
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