MicroRNA-155 modulates Th1 and Th17 cell differentiation and is associated with multiple sclerosis and experimental

Jing Zhang1, Ye Cheng1, Wei Cui1

  • 1The Department of Neurology of the Second Hospital of Hebei Medical University, China.

Journal of Neuroimmunology
|December 17, 2013
PubMed

Insights

MicroRNA-155 (miR-155) drives autoimmune disease severity in multiple sclerosis and experimental autoimmune encephalomyelitis by promoting inflammatory T cell responses. Reducing miR-155 may offer a novel therapeutic strategy for these conditions.

Area of Science:

  • Immunology
  • Molecular Biology
  • Neuroscience

Background:

  • Noncoding microRNAs (miRNAs) play a role in immune system regulation.
  • Dysregulation of miRNAs is implicated in autoimmune diseases like multiple sclerosis (MS).

Purpose of the Study:

  • To investigate the role of microRNA-155 (miR-155) in the pathogenesis of multiple sclerosis (MS) and experimental autoimmune encephalomyelitis (EAE).
  • To determine if miR-155 can be a therapeutic target for MS.

Main Methods:

  • Correlative analysis of miR-155 expression with disease severity in MS patients and EAE mice.
  • In vivo knockdown and overexpression of miR-155 in EAE mouse models.
  • Analysis of T helper cell subsets (Th1 and Th17) and their inflammatory profiles.

Main Results:

  • miR-155 expression levels strongly correlated with disease severity in both MS patients and EAE mice.
  • Knockdown of miR-155 led to reduced Th1 and Th17 cells and attenuated EAE.
  • Overexpression of miR-155 resulted in increased Th1 and Th17 cells and exacerbated EAE.
  • miR-155 was found to promote the development of inflammatory Th17/Th1 cell subsets.

Conclusions:

  • miR-155 significantly contributes to susceptibility to EAE by modulating inflammatory T cell responses.
  • miR-155 represents a potential therapeutic target for multiple sclerosis and related autoimmune conditions.

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