Literature DB >> 7189001

Optic neuritis and chronic relapsing experimental allergic encephalomyelitis: relationship to clinical course and comparison with multiple sclerosis.

C S Raine, U Traugott, R B Nussenblatt, S H Stone.   

Abstract

Optic nerve tissue from strain 13 guinea pigs sensitized for chronic (relapsing) experimental allergic encephalomyelitis has been examined up to 3 years postinoculation. The changes were compared with the clinical history in each case, with lesions occurring elsewhere in the central nervous system and with optic nerve tissue from a single case of chronic multiple sclerosis. In chronic experimental allergic encephalomyelitis was found that optic neuritis was a consistent finding. Active lesions in the optic nerve were a feature of animals sampled up to 4 months postinoculation. Unlike lesions in the spinal cord, changes occurring in long term animals did not parallel clinical signs. The absence of active lesions in long term animals was apparently not due to a resistance to recurrent disease on the part of the tissue since a second challenge with central nervour system tissue was capable of producing active inflammation in the optic nerve. It appears, therefore, that in its unmanipulated state, chronic experimental allergic encephalomyelitis is more a disease of the spinal cord. Optic nerve changes in the case of multiple sclerosis did not compare well with the guinea pit lesions--discrepancies which we speculate as being related to differences in anatomy, age, species, and longevity of the disease process (among others), rather than a difference in pathogenesis.

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Year:  1980        PMID: 7189001

Source DB:  PubMed          Journal:  Lab Invest        ISSN: 0023-6837            Impact factor:   5.662


  7 in total

1.  Experimental allergic encephalomyelitis in rhesus monkeys: II. Treatment of EAE with anti-T lymphocyte subset monoclonal antibodies.

Authors:  R Van Lambalgen; M Jonker
Journal:  Clin Exp Immunol       Date:  1987-05       Impact factor: 4.330

2.  Experimental allergic encephalomyelitis: modification of optic nerve pathology by antecedent virus infection.

Authors:  A J Suckling; N R Wilson; M G Rumsby
Journal:  Acta Neuropathol       Date:  1982       Impact factor: 17.088

Review 3.  Experimental autoimmune encephalomyelitis (EAE) as a model for multiple sclerosis (MS).

Authors:  Cris S Constantinescu; Nasr Farooqi; Kate O'Brien; Bruno Gran
Journal:  Br J Pharmacol       Date:  2011-10       Impact factor: 8.739

4.  Optic Neuritis: A Model for the Immuno-pathogenesis of Central Nervous System Inflammatory Demyelinating Diseases.

Authors:  Gregory F Wu; Chelsea R Parker Harp; Kenneth S Shindler
Journal:  Curr Immunol Rev       Date:  2015

5.  Noninvasive assessments of optic nerve neurodegeneration in transgenic mice with isolated optic neuritis.

Authors:  Venu Talla; Cui Yang; Gerry Shaw; Vittorio Porciatti; Rajeshwari D Koilkonda; John Guy
Journal:  Invest Ophthalmol Vis Sci       Date:  2013-07-01       Impact factor: 4.799

6.  Damage to the optic chiasm in myelin oligodendrocyte glycoprotein-experimental autoimmune encephalomyelitis mice.

Authors:  Sheryl L Herrera; Vanessa L Palmer; Heather Whittaker; Blair Cardigan Smith; Annie Kim; Angela E Schellenberg; Jonathan D Thiessen; Richard Buist; Marc R Del Bigio; Melanie Martin
Journal:  Magn Reson Insights       Date:  2014-11-09

7.  Myelin oligodendrocyte glycoprotein-specific T cell receptor transgenic mice develop spontaneous autoimmune optic neuritis.

Authors:  Estelle Bettelli; Maria Pagany; Howard L Weiner; Christopher Linington; Raymond A Sobel; Vijay K Kuchroo
Journal:  J Exp Med       Date:  2003-05-05       Impact factor: 14.307

  7 in total

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