Identification and validation of mutual hub genes in idiopathic pulmonary fibrosis and rheumatoid arthritis-associated usual interstitial pneumonia.

Objectives: The study aims at exploring common hub genes and pathways in idiopathic pulmonary fibrosis (IPF) and rheumatoid arthritis-associated usual interstitial pneumonia (RA-UIP) through integrated bioinformatics analyses.

Methods: The GSE199152 dataset containing lung tissue samples from IPF and RA-UIP patients was acquired from the Gene Expression Omnibus (GEO) database. The identification of overlapping differentially expressed genes (DEGs) in IPF and RA-UIP was carried out through R language.

Screening and validation of differentially expressed genes in polymyositis.

Background: Polymyositis (PM), a prevalent inflammatory myopathy, currently lacks defined pathogenic mechanism. To illuminate its pathogenesis, we integrated bioinformatics and clinical specimens to examine potential aberrant gene expression patterns and their localization.

Methods: We obtained GSE128470 and GSE3112 dataset from the Gene Expression Omnibus, performed Gene Set Enrichment Analysis (GSEA) and immune infiltration analysis using CiberSort, identified differentially expressed genes with Limma, conducted functional annotation and Kyoto Encyclopedia of Genes and Genomes (KEGG) pathway enrichment analysis, constructed a Protein-Protein Interaction network, and identified hub genes using Cytoscape.

CD4LAG3T cells are decreased in SSc-ILD and affect fibroblast mesenchymal transition by TGF-β3.

Pulmonary fibrosis frequently occurs in rheumatic conditions, particularly systemic sclerosis-associated interstitial lung disease (SSc-ILD). The pathology involves cell transformation into interstitial structures and collagen accumulation. CD4LAG3T cells, known for immune inhibition, are relevant in autoimmunity.