Long noncoding RNA FOXP1-DT modulates regulatory T cells in Graves' disease

Area of Science:

• Immunology
• Molecular Biology
• Genetics

Background:

• Regulatory T cells (Tregs) are crucial for immune homeostasis.
• Treg dysfunction is implicated in Graves' disease (GD) pathogenesis.
• The molecular mechanisms of Treg dysregulation in GD are not fully understood.

Purpose of the Study:

• To investigate the role of the long noncoding RNA FOXP1-DT in Tregs from GD patients.
• To explore the relationship between FOXP1-DT, FOXP1 expression, and Treg levels in GD.

Main Methods:

• Recruitment of 15 GD patients and 15 healthy controls.
• Quantification of FOXP1-DT and FOXP1 expression in peripheral blood mononuclear cells.
• Correlation analysis with clinical parameters and Treg cell frequency.
• FOXP1-DT silencing experiments.
• Receiver Operating Characteristic (ROC) curve analysis.

Main Results:

• FOXP1-DT expression was significantly decreased in GD patients.
• Decreased FOXP1-DT correlated inversely with thyroid-stimulating hormone receptor antibody levels.
• FOXP1 expression and Treg cell proportion were reduced in GD patients and positively correlated with FOXP1-DT.
• Silencing FOXP1-DT reduced FOXP1 expression and Treg proportion.
• FOXP1-DT demonstrated potential as a biomarker for GD.

Conclusions:

• Downregulated FOXP1-DT may contribute to GD pathogenesis by disrupting FOXP1-mediated Treg homeostasis.
• FOXP1-DT warrants further investigation as a potential therapeutic target and diagnostic biomarker for Graves' disease.