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Elevated ATG5 expression in autoimmune demyelination and multiple sclerosis

Academic Article
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Overview

authors

  • Alirezaei, M.
  • Fox, H. S.
  • Flynn, C. T.
  • Moore, C. S.
  • Hebb, A. L. O.
  • Frausto, R. F.
  • Bhan, V.
  • Kiosses, W. B.
  • Whitton, J. Lindsay
  • Robertson, G. S.
  • Crocker, S. J.

publication date

  • February 2009

journal

  • Autophagy  Journal

abstract

  • Multiple sclerosis (MS) is an inflammatory central nervous system (CNS) disorder characterized by T cell-mediated demyelination. In MS, prolonged T cell survival and increased T cell proliferation have been linked to disease relapse and progression. Recently, the autophagy-related gene 5 (Atg5) has been shown to modulate T cell survival. In this study, we examined the expression of Atg5 using both a mouse model of autoimmune demyelination as well as blood and brain tissues from MS cases. Quantitative real-time PCR analysis of RNA isolated from blood samples of experimental autoimmune encephalomyelitis (EAE) mice revealed a strong correlation between Atg5 expression and clinical disability.Analysis of protein extracted from these cells confirmed both upregulation and post-translational modification of Atg5, the latter of which was positively correlated with EAE severity. Analysis of RNA extracted from T cells isolated by negative selection indicated that Atg5 expression was significantly elevated in individuals with active relapsing-remitting MS compared to non-diseased controls. Brain tissue sections from relapsing-remitting MS cases examined by immunofluorescent histochemistry suggested that encephalitogenic T cells are a source of Atg5 expression in MS brain samples. Together these data suggest that increased T cell expression of Atg5 may contribute to inflammatory demyelination in MS.

subject areas

  • Adult
  • Aged
  • Animals
  • Brain
  • Encephalomyelitis, Autoimmune, Experimental
  • Female
  • Gene Expression Regulation
  • Humans
  • Male
  • Mice
  • Microtubule-Associated Proteins
  • Middle Aged
  • Multiple Sclerosis
  • Postmortem Changes
  • RNA, Messenger
  • T-Lymphocytes
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Research

keywords

  • Atg5
  • CNS
  • EAE
  • T cell
  • apoptosis
  • autoimmune
  • autophagy
  • encephalomyelitis
  • multiple sclerosis
  • neuroinflammation
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Identity

PubMed Central ID

  • PMC2779564

International Standard Serial Number (ISSN)

  • 1554-8627

Digital Object Identifier (DOI)

  • 10.4161/auto.5.2.7348

PubMed ID

  • 19066443
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Additional Document Info

start page

  • 152

end page

  • 158

volume

  • 5

issue

  • 2

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