Christopher Lock1, 9, Guy Hermans1, 9, Rosetta Pedotti1, 9, Andrea Brendolan2, 9, Eric Schadt4, Hideki Garren1, Annette Langer-Gould1, Samuel Strober2, Barbara Cannella7, John Allard8, Paul Klonowski8, Angela Austin8, Nagin Lad8, Naftali Kaminski6, Stephen J. Galli3, Jorge R. Oksenberg5, Cedric S. Raine7, Renu Heller8
& Lawrence Steinman11
Departments of Neurology and Neurological Sciences, Beckman Center, Stanford University, Stanford, California, USA
2
Medicine, Stanford University, Stanford, California, USA
3
Pathology, Stanford University, Stanford, California, USA
4
Informatics, Rosetta Inpharmatics, Kirkland, Washington, USA
5
Departments of Neurology, San Francisco, California, USA
6
Lung Biology Center and Cardiovascular Research Institute, University of California at San Francisco School of Medicine, San Francisco, California, USA
7
Department of Pathology (Neuropathology) and Neurology, Albert Einstein College of Medicine, Bronx, New York, USA
8
Roche Bioscience, Palo Alto, California, USA
9
C.L., G.H., R.P. and A.B. contributed equally to this study.
Correspondence should be addressed to Renu Heller rheller@stanford.edu or Lawrence Steinman steinman@stanford.edu
and associated downstream pathways. Comparison of two poles of MS pathology—acute lesions with inflammation versus 'silent' lesions without inflammation—revealed differentially transcribed genes. Some products of these genes were chosen as targets for therapy of experimental autoimmune encephalomyelitis (EAE) in mice. Granulocyte colony-stimulating factor is upregulated in acute, but not in chronic, MS lesions, and the effect on ameliorating EAE is more pronounced in the acute phase, in contrast to knocking out the immunoglobulin Fc receptor common 
