May 2008
Volume 49, Issue 13
Free
ARVO Annual Meeting Abstract  |   May 2008
Immune Privilege Ameliorates Murine Experimental Autoimmune Optic Neuritis Induced With Myelin/Oligodendrocyte Glycoprotein
Author Affiliations & Notes
  • Y. Matsunaga
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • T. Kezuka
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • Y. Usui
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • R. Matsuda
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • N. Yamakawa
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • J. Ma
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • M. Takeuchi
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • H. Goto
    Ophthalmology, Tokyo Medical University, Shinjuku-ku, Japan
  • Footnotes
    Commercial Relationships  Y. Matsunaga, None; T. Kezuka, None; Y. Usui, None; R. Matsuda, None; N. Yamakawa, None; J. Ma, None; M. Takeuchi, None; H. Goto, None.
  • Footnotes
    Support  None.
Investigative Ophthalmology & Visual Science May 2008, Vol.49, 793. doi:https://doi.org/
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    • Get Citation

      Y. Matsunaga, T. Kezuka, Y. Usui, R. Matsuda, N. Yamakawa, J. Ma, M. Takeuchi, H. Goto; Immune Privilege Ameliorates Murine Experimental Autoimmune Optic Neuritis Induced With Myelin/Oligodendrocyte Glycoprotein. Invest. Ophthalmol. Vis. Sci. 2008;49(13):793. doi: https://doi.org/.

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

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Abstract

Purpose: : To investigate whether injection of antigen into the anterior chamber of the eye (anterior chamber-associated immune deviation: ACAID) ameliorates both murine experimental autoimmune optic neuritis (EON) and experimental autoimmune encephalomyelitis (EAE).

Methods: : Myelin/oligodendrocyte glycoprotein derived peptide 35-55 (MOG35-55) was injected into the anterior chamber (AC) of B6 mice. After 5 days, mice were immunized with 200 ug of MOG35-55 in CFA and were injected intraperitoneally with 1ug of pertussis toxin. Diagnosis of EAE was made on the clinical symptoms of the disease. On day 13 after immunization, MOG35-55-specific delayed hypersensitivity (DH) were measured. On day 14 after immunization, animals were sacrificed, and assessed the extent of EON pathologically. The severity of EON in each eye was scored on scale of 0 to 3.

Results: : MOG35-55 injected into the AC significantly reduced DH in MOG35-55 immunized mice. As well as the results of DH, EAE induced by immunization with MOG35-55 were ameliorated by AC injection of MOG35-35. Immunization of B6 mice with MOG35-55 also indicated EON characterized by lymphocyte infiltration into retrobulber optic nerves with intact retina, and the incidence of EON was 100%. AC injection with MOG35-55 reduced the incidence to 70%, and the severity of EON was also ameliorated from the average score 1.6 to 0.6.

Conclusions: : Immunization with MOG35-55 developed EON as well as EAE, and ACAID induced by AC injection with MOG35-55 ameliorated both of the diseases.

Keywords: optic nerve • ACAID • inflammation 
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