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Immunity to the Extracellular Domain of Nogo-A Modulates Experimental Autoimmune Encephalomyelitis¹

Paulo Fontoura^2,*,¶, Peggy P. Ho^*, Jason DeVoss^*, Binhai Zheng, Byung J. Lee^*, Brian A. Kidd, Hideki Garren^||, Raymond A. Sobel, William H. Robinson, Marc Tessier-Lavigne and Lawrence Steinman^*

Departments of ^* Neurology and Neurological Sciences, School of Medicine, Biological Sciences, Howard Hughes Medical Institute, Pathology, School of Medicine, and Division of Immunology and Rheumatology, Department of Medicine, Stanford University, Stanford, CA 94305; ^¶ Gulbenkian Science Institute, Oeiras, Portugal; and ^|| Bayhill Therapeutics, Palo Alto, CA 94303

Nogo-66, the extracellular 66 aa loop of the Nogo-A protein found in CNS myelin, interacts with the Nogo receptor and has been proposed to mediate inhibition of axonal regrowth. It has been shown that immunization with Nogo-A promotes recovery in animal models of spinal cord injury through induction of Ab production. In this report, studies were performed to characterize the immune response to Nogo-66 and to determine the role of Nogo in experimental autoimmune encephalomyelitis (EAE). Immunization of EAE-susceptible mouse strains with peptides derived from Nogo-66 induced a CNS immune response with clinical and pathological similarities to EAE. The Nogo-66 peptides elicited strong T cell responses that were not cross-reactive to other encephalitogenic myelin Ags. Using a large scale spotted microarray containing proteins and peptides derived from a wide spectrum of myelin components, we demonstrated that Nogo-66 peptides also generated a specific Ab response that spreads to several other encephalitogenic myelin Ags following immunization. Nogo-66-specific T cell lines ameliorated established EAE, via Nogo-66-specific Th2 cells that entered the CNS. These results indicate that some T cell and B cell immune responses to Nogo-66 are associated with suppression of ongoing EAE, whereas other Nogo-66 epitopes can be encephalitogenic.

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The JI 2004 173: 6499-6500. [Full Text]  

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