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Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis
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Modeling Multiple Sclerosis in the Two Sexes: MOG35-55-Induced Experimental Autoimmune Encephalomyelitis

Published on: October 13, 2023

Peroxisome proliferator-activated receptor delta agonists inhibit T helper type 1 (Th1) and Th17 responses in

Saravanan Kanakasabai1, Wanida Chearwae, Crystal C Walline

  • 1Neuroscience Research Laboratory, Methodist Research Institute, Indianapolis, IN 46202, USA.

Immunology
|April 22, 2010
PubMed

Insights

PPARdelta agonists effectively treat experimental autoimmune encephalomyelitis (EAE), a model for multiple sclerosis (MS). These compounds reduce key inflammatory markers, suggesting a new therapeutic avenue for MS and other autoimmune diseases.

Area of Science:

  • Neuroimmunology
  • Molecular Endocrinology

Background:

  • Multiple sclerosis (MS) is a debilitating neurological disorder with unknown etiology and no cure.
  • Experimental autoimmune encephalomyelitis (EAE) serves as a T-cell-mediated autoimmune disease model for MS, involving CNS inflammation and myelin destruction.
  • Peroxisome proliferator-activated receptors (PPARs) are nuclear receptors regulating cellular processes; their agonists show therapeutic potential in inflammatory conditions.

Purpose of the Study:

  • To investigate the efficacy of PPARdelta agonists in ameliorating experimental autoimmune encephalomyelitis (EAE).
  • To elucidate the immunomodulatory mechanisms of PPARdelta agonists in the context of EAE and potential MS treatment.

Main Methods:

  • Administration of PPARdelta agonists (GW501516 and L165041) to MOGp35-55-induced EAE in C57BL/6 mice.
  • Assessment of inflammatory cytokine profiles, including interferon-gamma (IFN-γ), interleukin-17 (IL-17), IL-12, IL-23, IL-4, and IL-10, in the central nervous system (CNS) and lymphoid organs.
  • Evaluation of the impact on T helper type 1 (Th1) and Th17 cell responses.

Main Results:

  • PPARdelta agonists GW501516 and L165041 significantly ameliorated EAE.
  • These agonists suppressed the production of IFN-γ and IL-17 by Th1 and Th17 cells, respectively.
  • Treatment led to decreased IL-12 and IL-23 levels and increased IL-4 and IL-10 expression in the CNS and lymphoid organs.

Conclusions:

  • PPARdelta agonists modulate Th1 and Th17 immune responses in the EAE model.
  • These findings support the potential therapeutic application of PPARdelta agonists for treating multiple sclerosis and other autoimmune diseases.

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