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MicroRNA let-7g-5p alleviates murine collagen-induced arthritis by inhibiting Th17 cell differentiation

Pei Yang1, Mingfei Zhang1, Xiang Wang1

  • 1Jiangsu Provincial Key Laboratory of Pharmacology and Safety Evaluation of Material Medical, School of Pharmacy, Nanjing University of Chinese Medicine, Nanjing 210023, PR China.

Biochemical Pharmacology
|January 29, 2020
PubMed

Insights

MicroRNA let-7g-5p is reduced in rheumatoid arthritis (RA), promoting T helper 17 (Th17) cells. Restoring let-7g-5p in mice with collagen-induced arthritis (CIA) reduced disease severity by inhibiting Th17 cell differentiation.

Area of Science:

  • Immunology
  • Molecular Biology
  • Rheumatology

Background:

  • Rheumatoid arthritis (RA) is a complex systemic autoimmune disease.
  • T helper 17 (Th17) cells play a critical role in RA pathogenesis.
  • The precise role of microRNAs (miRNAs) in Th17 cell regulation in RA remains unclear.

Purpose of the Study:

  • To investigate the role of miRNA let-7g-5p in Th17 cell differentiation and function in rheumatoid arthritis.
  • To evaluate the therapeutic potential of let-7g-5p in a mouse model of RA.

Main Methods:

  • Quantitative analysis of let-7g-5p expression in RA patients and a collagen-induced arthritis (CIA) mouse model.
  • In vitro assessment of let-7g-5p's effect on Th17 cell differentiation and function.
  • In vivo administration of let-7g-5p mimics in CIA mice to assess therapeutic efficacy.

Main Results:

  • let-7g-5p expression was significantly decreased in RA patients and CIA mice, correlating with increased Th17 cell populations.
  • let-7g-5p was confirmed to inhibit Th17 cell differentiation and function in vitro.
  • Treatment with let-7g-5p mimics ameliorated disease severity and reduced Th17 cell frequency in CIA mice.

Conclusions:

  • let-7g-5p acts as a negative regulator of Th17 cell differentiation.
  • let-7g-5p ameliorates collagen-induced arthritis by suppressing Th17 cell development.
  • let-7g-5p represents a potential novel therapeutic strategy for treating RA and other autoimmune diseases.
Keywords:
Collagen‑induced arthritisLet-7g-5pRheumatoid arthritisTh17 cells

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