May 2005
Volume 46, Issue 13
ARVO Annual Meeting Abstract  |   May 2005
Establishment of an Autoimmune Optic Neuritis Model in C57Bl/6 Mouse
Author Affiliations & Notes
  • Y. Peng
    Opthalmology, University of Louisville, Louisville, KY
  • H. Shi
    Opthalmology, University of Louisville, Louisville, KY
  • H.J. Kaplan
    Opthalmology, University of Louisville, Louisville, KY
  • H. Shao
    Opthalmology, University of Louisville, Louisville, KY
  • D. Sun
    Opthalmology, University of Louisville, Louisville, KY
  • Footnotes
    Commercial Relationships  Y. Peng, None; H. Shi, None; H.J. Kaplan, None; H. Shao, None; D. Sun, None.
  • Footnotes
    Support  NIH grants EY014–366, EY12974, EY14599; NMSS grant RG3413A4; RPB award
Investigative Ophthalmology & Visual Science May 2005, Vol.46, 1000. doi:
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    • Get Citation

      Y. Peng, H. Shi, H.J. Kaplan, H. Shao, D. Sun; Establishment of an Autoimmune Optic Neuritis Model in C57Bl/6 Mouse . Invest. Ophthalmol. Vis. Sci. 2005;46(13):1000.

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      © ARVO (1962-2015); The Authors (2016-present)

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Abstract: : Purpose: The optic nerve is a common site of tissue damage in multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE). To determine the relationship between optic neuritis (ON) and EAE, we examined the incidence of ON in C57Bl/6 (B6) mice immunized with a myelin oligodendrocyte/glycoprotein (MOG)–derived peptide or injected with MOG–specific T cells, which are known to induce EAE. Methods: Mice were immunized with MOG35–55 or MOG40–54 peptides emulsified in complete Freund's adjuvant (CFA). Pertussis toxin (PTX) was injected intraperitoneally 1 day before and after immunization. For disease induction by adoptive transfer of primed cells, donor C57BL/6 mice were received with T–cell blasts (1–6 x 10(6)/mouse). Both EAE and ON were observed by either clinical signs or histology. Results: A high proportion of B6 mice treated using either protocol developed ON. The most severe inflammation was observed in the adoptively transferred mice. The induced ON was most frequently bilateral. Determination of disease susceptibility induced by immunization with lower doses of the MOG peptide or with truncated MOG peptides or by transfer of different numbers of MOG–specific T cells showed that, in each of these induced diseases, both association and dissociation of EAE and ON was seen, indicating the possibility that different MOG–specific T cell subsets might be involved. Conclusions: Different MOG–specific T–cell subsets might be involved in the pathogenesis of EAE and ON. Since MS is thought to be the human analog of EAE and since ON is a frequent presenting sign in patients with MS, a better understanding of the pathogenesis of ON following induction by MOG may have important diagnostic and therapeutic implications.

Keywords: neuro-ophthalmology: optic nerve • pathology: experimental • immunomodulation/immunoregulation 

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