The aberrant expression of microRNAs and correlations with T cell subsets in patients with immune thrombocytopenia

Lu Liu1, Mingqiang Hua1, Chuanfang Liu1

  • 1Department of Hematology, Qilu Hospital, Shandong University, Jinan, China.

Oncotarget
|November 2, 2016
PubMed

Insights

Immune thrombocytopenia (ITP) involves altered microRNA and T helper cell levels. MiR-146a may regulate T regulatory cells and influence ITP, showing potential as a therapeutic target.

Area of Science:

  • Immunology
  • Molecular Biology
  • Hematology

Background:

  • Autoimmune diseases like immune thrombocytopenia (ITP) involve complex immune dysregulation.
  • The roles of microRNAs (miRNAs) and T helper (Th) cells in ITP pathogenesis are not fully understood.

Purpose of the Study:

  • To investigate immune-related miRNA expression profiles and Th cell frequencies in ITP patients.
  • To explore the regulatory effect of miR-146a on Th cell differentiation in ITP.

Main Methods:

  • Quantification of seven immune-related miRNAs and four Th cell subsets (Th1, Th2, Th17, Treg) in peripheral blood mononuclear cells (PBMCs) from ITP patients and healthy controls.
  • Measurement of platelet autoantibodies using the MAIPA assay.
  • In vitro evaluation of miR-146a's effect on Th differentiation using agomir and dexamethasone (DEX).

Main Results:

  • Lower expression of miR-146a, miR-326, and miR-142-3p observed in ITP patients compared to controls.
  • Increased frequencies of Th17 and Th22 cells, with decreased Treg cells, in ITP patients.
  • Negative correlation between miR-142-3p/miR-146a and Th17 cells; positive correlation between miR-146a and Treg cells/platelet counts.
  • Upregulated miR-146a promoted Th17 and Treg differentiation and was induced by DEX in ITP PBMCs.

Conclusions:

  • ITP is characterized by distinct immune-related miRNA expression profiles and altered Th cell populations.
  • miR-146a plays a significant role in regulating Treg differentiation and function in ITP.
  • miR-146a modulation presents a potential therapeutic strategy for ITP.