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Infection with a recombinant vaccinia virus encoding myelin proteolipid protein causes suppression of chronic relapsing-remitting experimental allergic encephalomyelitis

Academic Article
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Overview

authors

  • Wang, L. Y.
  • Theil, D. J.
  • Whitton, J. Lindsay
  • Fujinami, R. S.

publication date

  • May 1999

journal

  • Journal of Neuroimmunology  Journal

abstract

  • Mice infected with a recombinant vaccinia virus (VVplp) encoding the myelin proteolipid protein (PLP) and then challenged with the encephalitogenic peptide, PLP139-151, developed a more severe acute attack vs. control mice. Following this initial acute attack, vaccinated mice had significantly less clinical disease (relapses) than control vaccinated or mock vaccinated mice. Control mice developed a relapsing-remitting disease with severe clinical relapses. During the remission state in VVplp vaccinated mice, histopathologic changes were markedly reduced in the central nervous system (CNS) vs. control vaccinated or unvaccinated mice. Inflammation was mainly limited to the meninges with a reduction of mononuclear cells in the parenchyma of the spinal cord in VVplp vaccinated and PLP139-151 challenged mice vs. control mice where inflammatory changes with demyelination was observed. During the remission period an increase in IL-4 was seen. In addition, there was significantly less T cell proliferation to PLP139-151 that was confirmed by an in vivo measurement of T cell reactivity, DTH responses. This suggests that the almost permanent remission state was dictated by a decreased responsiveness to PLP139-151 in VVplp vaccinated mice.

subject areas

  • Acute Disease
  • Animals
  • Chronic Disease
  • Cytokines
  • Encephalomyelitis, Autoimmune, Experimental
  • Epitopes
  • Female
  • Mice
  • Mice, Inbred Strains
  • Myelin Proteolipid Protein
  • Myelin Sheath
  • Peptide Fragments
  • Recombination, Genetic
  • Recurrence
  • Time Factors
  • Vaccination
  • Vaccinia
  • Vaccinia virus
  • Viral Vaccines
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Identity

International Standard Serial Number (ISSN)

  • 0165-5728

Digital Object Identifier (DOI)

  • 10.1016/S0165-5728(99)00020-X

PubMed ID

  • 10337913
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Additional Document Info

start page

  • 148

end page

  • 157

volume

  • 96

issue

  • 2

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