The Journal of Experimental Medicine
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Published online 9 June 2003 doi:10.1084/jem.20021546
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© Rockefeller University Press, 0022-1007/2003/6/1657 $5.00
The Journal of Experimental Medicine, Volume 197, Number 12, 1657-1666

CD36 Mediates the Innate Host Response to ß-Amyloid

Joseph B. El Khoury1,2, Kathryn J. Moore3, Terry K. Means1, Josephine Leung1, Kinya Terada4, Michelle Toft1, Mason W. Freeman3 and Andrew D. Luster1

1 Center for Immunology and Inflammatory Diseases, Division of Rheumatology, Allergy, and Immunology
2 Division of Infectious Diseases, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129
3 Lipid Metabolism Unit, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129
4 Neurosurgical Service, Massachusetts General Hospital, Harvard Medical School, Charlestown, MA 02129

Address correspondence to Andrew D. Luster, Center for Immunology and Inflammatory Diseases, Massachusetts General Hospital, CNY 149 13th Street, Room 8301, Charlestown, MA 02129. Phone: 617-726-5710; Fax: 617-726-5651; E-mail: luster{at}helix.mgh.harvard.edu

Accumulation of inflammatory microglia in Alzheimer's senile plaques is a hallmark of the innate response to ß-amyloid fibrils and can initiate and propagate neurodegeneration characteristic of Alzheimer's disease (AD). The molecular mechanism whereby fibrillar ß-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 ß-amyloid fibrils in vitro. We report here that microglia and macrophages, isolated from CD36 null mice, had marked reductions in fibrillar ß-amyloid–induced secretion of cytokines, chemokines, and reactive oxygen species. Intraperitoneal and stereotaxic intracerebral injection of fibrillar ß-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 ß-amyloid, and imply that CD36 plays a key role in the proinflammatory events associated with AD.

Key Words: microglia • scavenger receptor • Alzheimer's disease • chemokine • reactive oxygen species


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