| First Author | El Khoury JB | Year | 2003 |
| Journal | J Exp Med | Volume | 197 |
| Issue | 12 | Pages | 1657-66 |
| PubMed ID | 12796468 | Mgi Jnum | J:120662 |
| Mgi Id | MGI:3707627 | Doi | 10.1084/jem.20021546 |
| Citation | El Khoury JB, et al. (2003) CD36 mediates the innate host response to beta-amyloid. J Exp Med 197(12):1657-66 |
| abstractText | Accumulation of inflammatory microglia 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 microglia 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. |
