Nature Medicine
- 12, 138 - 143 (2005)
Published online: 11 December 2005; | doi:10.1038/nm1344
Lipid microarrays identify key mediators of autoimmune brain inflammationJennifer L Kanter1, 2, Sirisha Narayana2, Peggy P Ho2, Ingrid Catz3, Kenneth G Warren3, Raymond A Sobel4, 6, Lawrence Steinman2 & William H Robinson5, 61
Department of Microbiology and Immunology, Stanford University School of Medicine, 279 Campus Drive, Stanford, California 94305, USA. 2
Department of Neurology and Neurological Sciences, Stanford University School of Medicine, 279 Campus Drive, Stanford, California 94305, USA. 3
Department of Medicine, University of Alberta 9-101 Clinical Sciences Building, Edmonton, Alberta, Canada. 4
Department of Pathology, Stanford University School of Medicine, 269 Campus Drive, Stanford, California 94305, USA. 5
Division of Immunology and Rheumatology, Stanford University School of Medicine, 269 Campus Drive, Stanford, California 94305, USA. 6
Geriatric Research, Education and Clinical Center, Palo Alto VA Health Care System, 3801 Miranda Avenue, Palo Alto, California 94304, USA.
Correspondence should be addressed to William H Robinson wrobins@stanford.edu Recent studies suggest that increased T-cell and autoantibody reactivity to lipids may be present in the autoimmune demyelinating disease multiple sclerosis. To perform large-scale multiplex analysis of antibody responses to lipids in multiple sclerosis, we developed microarrays composed of lipids present in the myelin sheath, including ganglioside, sulfatide, cerebroside, sphingomyelin and total brain lipid fractions. Lipid-array analysis showed lipid-specific antibodies against sulfatide, sphingomyelin and oxidized lipids in cerebrospinal fluid (CSF) derived from individuals with multiple sclerosis. Sulfatide-specific antibodies were also detected in SJL/J mice with acute experimental autoimmune encephalomyelitis (EAE). Immunization of mice with sulfatide plus myelin peptide resulted in a more severe disease course of EAE, and administration of sulfatide-specific antibody exacerbated EAE. Thus, autoimmune responses to sulfatide and other lipids are present in individuals with multiple sclerosis and in EAE, and may contribute to the pathogenesis of autoimmune demyelination.
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