# Differential expression profiles of lncRNAs and a preliminary study on the mechanism of lncRNA FAM225A in triple seronegative myasthenia gravis

## TL;DR

This study identifies differentially expressed lncRNAs in triple-seronegative myasthenia gravis and explores the role of lncRNA FAM225A in disease severity and immune imbalance.

## Contribution

The first study to investigate lncRNA FAM225A's role in triple-seronegative MG and its potential as a biomarker and therapeutic target.

## Key findings

- 385 differentially expressed mRNAs and 361 lncRNAs were identified in triple-seronegative MG patients.
- LncRNA FAM225A is downregulated and negatively correlates with disease severity in triple-seronegative MG.
- FAM225A influences Th1/Th2 imbalance by targeting hsa-miR-150-5p in triple-seronegative MG pathogenesis.

## Abstract

Triple-seronegative (Triple-SN) myasthenia gravis (MG) is a subtype of MG, and its diagnosis and treatment are challenging. Our study aims to discover new biomarkers and potential therapeutic targets and explore the preliminary mechanisms of triple-SN MG.

Peripheral blood mononuclear cells (PBMCs) were collected from 15 patients with triple-SN MG who were newly diagnosed with the disease and 15 healthy controls. Various experimental techniques and analysis methods, such as PBMC isolation, microarray analysis, dual-luciferase reporter assay, quantitative real-time polymerase chain reaction (qRT-PCR), cell culture, and transfection, were used.

Our study identified 385 differentially expressed genes (DEmRNAs) and 361 differentially expressed lncRNAs (DElncRNAs) in triple-SN MG. Notably, lncRNA FAM225A, one of the top five downregulated DElncRNAs, was verified to decreased and negatively correlated with the clinical severity of triple-SN MG. Functional enrichment analysis, immune infiltration analysis and further experiments revealed that FAM225A affected the imbalance of Th1/Th2 by targeting hsa-miR-150-5p in the pathogenesis of triple-SN MG.

This study is the first to provide important clues for understanding the pathological mechanism of triple-SN MG, which might contribute to the discovery of novel diagnostic and therapeutic monitoring biomarkers and new targets for the treatment of triple-SN MG.