期刊
JOURNAL OF EXPERIMENTAL MEDICINE
卷 197, 期 12, 页码 1657-1666出版社
ROCKEFELLER UNIV PRESS
DOI: 10.1084/jem.20021546
关键词
microglia; scavenger receptor; Alzheimer's disease; chemokine; reactive oxygen species
资金
- NHLBI NIH HHS [R01 HL045098, R01 HL45098] Funding Source: Medline
- NIA NIH HHS [R01 AG020255, R01AG20255-01] Funding Source: Medline
- NIDDK NIH HHS [P01 DK50305, P01 DK050305] Funding Source: Medline
- NINDS NIH HHS [NS41330, K08 NS041330] Funding Source: Medline
Accumulation of inflammatory nucroglia in Alzheimer's senile plaques is a hallmark of the innate response to beta-amyloid fibrils and can initiate and propagate neurodegeneration characteristic of Alzheimer's disease (AD). The molecular mechanism whereby fibrillar beta-amyloid activates the inflammatory response has not been elucidated. CD36, a class B scavenger receptor, is expressed on nucroglia in normal and AD brains and binds to beta-amyloid fibrils in vitro. We report here that microglia and macrophages, isolated from CD36 null mice, had marked reductions in fibrillar beta-amyloid-induced secretion of cytokines, chemokines, and reactive oxygen species. Intraperitoneal and stereotaxic intracerebral injection of fibrillar beta-amyloid in CD36 null mice induced significantly less macrophage and microglial recruitment into the peritoneum and brain, respectively, than in wild-type mice. Our data reveal that CD36, a major pattern recognition receptor, mediates microglial and macrophage response to beta-amyloid, and imply that CD36 plays a key role in the proinflammatory events associated with AD.
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