# Zinc finger protein Y - linked as a potential biomarker for autoimmune hepatitis and multiple sclerosis which overlap with immune infiltration

## TL;DR

This study identifies ZFY as a potential biomarker for Autoimmune Hepatitis and Multiple Sclerosis, linking it to immune infiltration and the PI3K/Akt pathway.

## Contribution

The study discovers ZFY as a novel common biomarker for AIH and MS using bioinformatics and experimental validation.

## Key findings

- ZFY is significantly downregulated in both AIH and MS patients.
- ZFY is associated with immune cell infiltration and the PI3K/Akt pathway in both diseases.
- Experimental models confirm ZFY's diagnostic potential for AIH and MS.

## Abstract

Autoimmune Hepatitis (AIH) and Multiple Sclerosis (MS) are chronic inflammatory diseases with abnormal immune responses. This study aims to identify common biomarkers for AIH and MS using bioinformatics analysis. Gene expression data of AIH (GSE159676) and MS (GSE131279 and GSE131281) were obtained from the GEO database. Differentially Expressed Genes (DEGs) were identified using the limma package in R. Kyoto Encyclopedia of Genes and Genomes (KEGG) analysis, Protein-Protein Interaction (PPI) network, and machine learning algorithm Least Absolute Shrinkage and Selection Operator (LASSO) regression were used to evaluate potential biomarkers. The common biomarker gene Zinc Finger Protein Y-linked (ZFY) was identified. KEGG analysis showed significant enrichment of the Phosphatidylinositol 3-Kinase/Protein Kinase B (PI3K/Akt) pathway in both diseases. LASSO regression identified ZFY as a potential diagnostic marker, with decreased expression in both AIH and MS groups. Single-gene immune infiltration analysis indicated a significant association between ZFY expression and immune cell infiltration levels. Experimental validation in ConA-induced hepatitis and CPZ-mediated demyelination model mice further verified the diagnostic potential of ZFY. This study reveals the potential of ZFY as a biomarker for AIH and MS, highlighting its role in the PI3K/Akt pathway and immune infiltration. These findings provide new insights into the common pathological mechanisms of AIH and MS and suggest potential targets for future therapeutic strategies.