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A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model
11:03

A Cryo-pulverization Protocol for Processing Mouse Paws to Evaluate Molecular Pathways of Tissue Inflammation in a Collagen Induced Arthritis Model

Published on: October 30, 2019

Deacetylase inhibition increases regulatory T cell function and decreases incidence and severity of collagen-induced

Sandra J Saouaf1, Bin Li, Geng Zhang

  • 1Department of Pathology and Laboratory Medicine, University of Pennsylvania, Philadelphia, PA 19104-6082, USA.

Experimental and Molecular Pathology
|July 7, 2009
PubMed

Insights

Histone/protein deacetylase inhibitors (HDACi), like valproic acid (VPA), can treat autoimmune diseases by enhancing regulatory T cell (Treg) function and numbers. This study shows VPA reduces collagen-induced arthritis severity in mice.

Area of Science:

  • Immunology
  • Rheumatology
  • Pharmacology

Background:

  • Collagen-induced arthritis (CIA) is a mouse model for rheumatoid arthritis.
  • Histone/protein deacetylase inhibitors (HDACi) show promise in treating autoimmune diseases, but mechanisms are unclear.
  • Regulatory T cells (Tregs) are crucial for immune tolerance and are impaired in rheumatoid arthritis.

Purpose of the Study:

  • To investigate the effects of HDAC inhibitors on Treg function in the CIA model.
  • To explore the therapeutic potential of HDAC inhibitors in autoimmune disease.

Main Methods:

  • Mice were induced with collagen-induced arthritis (CIA).
  • Valproic acid (VPA), an HDAC inhibitor, was administered to CIA mice.
  • Treg numbers and suppressive function were assessed.
  • Disease incidence and severity were evaluated.

Main Results:

  • VPA significantly reduced CIA incidence and severity.
  • VPA treatment increased the suppressive function of CD4(+)CD25(+) Tregs.
  • VPA increased the numbers of CD25(+)FOXP3(+) Tregs in vivo.

Conclusions:

  • Clinically approved HDAC inhibitors like VPA may limit autoimmune disease progression.
  • HDAC inhibitors exert therapeutic effects possibly through enhancing FOXP3(+) Treg cell production and function.
  • Targeting Treg cells with HDAC inhibitors represents a potential therapeutic strategy for autoimmune disorders.

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