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Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
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MOG(35-55) i.v suppresses experimental autoimmune encephalomyelitis partially through modulation of Th17 and JAK/STAT

Zhilong Jiang1, Hongmei Li, Denise C Fitzgerald

  • 1Department of Neurology, Thomas Jefferson University, Philadelphia, PA 19107, USA.

European Journal of Immunology
|February 19, 2009
PubMed

Insights

Intravenous MOG peptide therapy prevents experimental autoimmune encephalomyelitis (EAE) by downregulating key inflammatory pathways. This immune tolerance involves reduced IL-17 production and altered signaling in immune cells, offering therapeutic potential for multiple sclerosis (MS).

Area of Science:

  • Immunology
  • Neuroscience
  • Molecular Biology

Background:

  • Experimental autoimmune encephalomyelitis (EAE) is a model for multiple sclerosis (MS).
  • Intravenous (i.v.) administration of encephalitogenic peptides can induce tolerance and prevent EAE.
  • The precise cellular and molecular mechanisms underlying i.v. tolerance in EAE remain incompletely understood, particularly concerning the IL-23/IL-17 pathway.

Purpose of the Study:

  • To investigate the effects of i.v. MOG(35-55) peptide administration on intracellular signaling pathways in an EAE model.
  • To determine the role of the IL-23/IL-17 system in MOG-induced i.v. tolerance.
  • To identify specific immune cell populations involved in mediating this tolerance.

Main Methods:

  • Induction of i.v. tolerance to EAE using MOG(35-55) peptide in a mouse model.
  • Analysis of intracellular signaling pathway phosphorylation (JAK/STAT, ERK1/2, NF-kappaB) in splenocytes and central nervous system tissue.
  • Measurement of IL-17 production and assessment of tolerance disruption by exogenous IL-17.
  • Flow cytometry to identify affected immune cell subsets (CD11b+, CD4+, CD8+, CD11c+).
  • Adoptive transfer of CD11b+ splenocytes from tolerized mice to recipients with actively induced EAE.

Main Results:

  • MOG(35-55) i.v. treatment significantly reduced phosphorylation of JAK/STAT-1, -4, ERK1/2, and NF-kappaBp65 in tolerized mice.
  • Reduced IL-17 production was observed in tolerized mice, and exogenous IL-17 partially broke tolerance.
  • Suppressed signaling pathways were primarily found in CD11b+ cells and to a lesser extent in CD4+, CD8+, and CD11c+ cells.
  • Adoptive transfer of CD11b+ splenocytes from tolerized mice delayed EAE onset and reduced clinical severity.

Conclusions:

  • Intravenous MOG peptide administration induces immune tolerance in EAE by modulating key intracellular signaling pathways, including JAK/STAT and NF-kappaB.
  • The IL-23/IL-17 system plays a critical role in EAE pathogenesis and is targeted by MOG-induced tolerance.
  • CD11b+ immune cells are important mediators of MOG-induced i.v. tolerance, suggesting novel therapeutic strategies for MS.

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