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Inhibition of transmethylation down-regulates CD4 T cell activation and curtails development of autoimmunity in a model system

Academic Article
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Overview

authors

  • Lawson, Brian
  • Manenkova, Y.
  • Ahamed, J.
  • Chen, X. R.
  • Zou, J. P.
  • BaccalĂ , Roberto
  • Theofilopoulos, Argyrios
  • Yuan, C.

publication date

  • April 2007

journal

  • Journal of Immunology  Journal

abstract

  • Transmethylation affects several cellular events, including T cell activation, and blockade of this pathway may curtail inflammatory/autoimmune responses. Here, we demonstrate that transmethylation inhibition by a novel reversible S-adenosyl-l-homocysteine hydrolase inhibitor leads to immunosuppression by reducing phosphorylation of several key proteins involved in TCR signaling, including Akt, Erk1/2, and NF-kappaB. Remarkably, this effect was largely restricted to CD4 T cells and correlated with reduced arginine methylation of Vav1, an essential guanine nucleotide exchange factor in T cell stimulation. Treatment with the transmethylation inhibitor averted, and even ameliorated, the CD4-mediated autoimmune disease, experimental autoimmune encephalomyelitis. The data suggest that transmethylation is required for CD4 T cell activation, and its inhibition may be a novel approach in the treatment of multiple sclerosis, and other CD4-mediated autoimmune diseases.

subject areas

  • Adenine
  • Adenosylhomocysteinase
  • Animals
  • Autoimmune Diseases
  • Butyrates
  • CD4-Positive T-Lymphocytes
  • Calcium
  • Down-Regulation
  • Encephalomyelitis, Autoimmune, Experimental
  • Enzyme Inhibitors
  • Female
  • Humans
  • Jurkat Cells
  • Lymphocyte Activation
  • Methylation
  • Mice
  • Proto-Oncogene Proteins c-vav
  • Receptors, Antigen, T-Cell
  • Signal Transduction
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Identity

International Standard Serial Number (ISSN)

  • 0022-1767

PubMed ID

  • 17404322
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Additional Document Info

start page

  • 5366

end page

  • 5374

volume

  • 178

issue

  • 8

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