Journal
JOURNAL OF IMMUNOLOGY
Volume 173, Issue 11, Pages 6981-6992Publisher
AMER ASSOC IMMUNOLOGISTS
DOI: 10.4049/jimmunol.173.11.6981
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Funding
- NHLBI NIH HHS [N01-HV-28183, N01 HV 28183] Funding Source: Medline
- NIAMS NIH HHS [K08 AR02133] Funding Source: Medline
- NIDDK NIH HHS [U19 DK61934] Funding Source: Medline
- NINDS NIH HHS [NS 046414, 5R01NS18235, 5F32NS11115] Funding Source: Medline
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Nogo-66, the extracellular 66 as 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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