Microglial activation resulting from CD40-CD40L interaction after β-amyloid stimulation

被引：310

作者：

Tan, J

Town, T

Paris, D

Mori, T

Suo, ZM

Crawford, F

Mattson, MP

Flavell, RA

Mullan, M

机构：

[1] Univ S Florida, Roskamp Inst, Tampa, FL 33613 USA

[2] Univ Kentucky, Sanders Brown Res Ctr Aging, Lexington, KY 40536 USA

[3] Univ Kentucky, Dept Anat & Neurobiol, Lexington, KY 40536 USA

[4] Yale Univ, Sch Med, Howard Hughes Med Inst, New Haven, CT 06520 USA

来源：

SCIENCE | 1999年 / 286卷 / 5448期

关键词：

D O I：

10.1126/science.286.5448.2352

中图分类号：

O [数理科学和化学]; P [天文学、地球科学]; Q [生物科学]; N [自然科学总论];

学科分类号：

07 ; 0710 ; 09 ;

摘要：

Alzheimer's disease (AD) has a substantial inflammatory component, and activated microglia may play a central role in neuronal degeneration, CD40 expression was increased on cultured microglia treated with freshly solublized amyloid-beta (A beta, 500 nanomolar) and on microglia from a transgenic murine model of AD (Tg APP(sw)). Increased tumor necrosis factor alpha production and induction of neuronal injury occurred when A beta-stimulated microglia were treated with CD40 ligand (CD40L), Microglia from Tg APP(sw) mice deficient for CD4OL demonstrated reduction in activation, suggesting that the CD40-CD40L interaction is necessary for A beta-induced microglial activation. Finally, abnormal tau phosphorylation was reduced in Tg APP(sw) animals deficient for CD40L, suggesting that the CD40-CD40L interaction is an early event in AD pathogenesis.

引用

页码：2352 / 2355

页数：4

共 28 条

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