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Characterization of murine experimental autoimmune encephalomyelitis induced by active immunization with a CD8 epitope of myelin oligodendrocyte glycoprotein

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Journal of Translational Medicine201210 (Suppl 3) :P26

  • Published:


  • Multiple Sclerosis
  • Experimental Autoimmune Encephalomyelitis
  • Multiple Sclerosis Patient
  • Myelin Oligodendrocyte Glycoprotein
  • Experimental Autoimmune Encephalomyelitis Model

Multiple sclerosis (MS) is an autoimmune, demyelinating and degenerative disease of the central nervous system (CNS). Anti-myelin CD4 T cells are strongly associated with disease development in several animal models of MS such as experimental autoimmune encephalomyelitis (EAE). However, CD8 T cells often outnumber CD4 T cells in the CNS parenchyma of MS patients and recent studies suggest that anti-myelin CD8 T cells may be also implicated. In order to better understand the contribution of pathogenic CD8 T cells, C57Bl/6 female mice were immunized with an epitope of myelin oligodendrocyte protein (MOG) specifically presented by MHC-I to CD8 T cells, as reported by Ford & Evavold in 2005. Only one third of these mice developed EAE with mild clinical signs. In contrast, mice immunized with MOG35-55 developed hindlimb paralysis, as expected for this model.

Proliferation and FACS analysis of T cell reactivity using splenocytes isolated from CD8 epitope-immunized mice confirmed the emergence of specific MOG-reactive CD8 T cells in vivo.

Immunohistochemical analysis of the spinal cord, cerebellum and optic nerve in mice that developed the first clinical signs indicates that CD8 T cells infiltrate the CNS white matter with a caudo-rostral gradient. Strikingly, the CD8 T cell infiltration is sparse compared with CD4 T cells. Sudan Black staining indicates myelin loss in the CNS white matter of these mice. Further characterization of the CNS T cells in this model is underway. Taken together, these data indicate that anti-myelin CD8 T cells can initiate EAE supporting an early role of CD8 T cells in MS pathogenesis. However, the development or phenotype of autoreactive T cells obtained with this immunization protocol is insufficient to trigger full EAE as compared with the classic EAE model using the CD4 (and CD8) epitope MOG35-55.

Supported by Region Pays-de-la-Loire (ABN).

Authors’ Affiliations

Institut National de la Santé et de la Recherche Médicale UMRS 1064 / ITUN, Nantes, France
L'UNAM, University of Nantes, Nantes, France


© Guillot et al; licensee BioMed Central Ltd. 2012

This article is published under license to BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.