PAX5 as a Common Diagnostic Marker in Inflammatory Bowel Disease and Rheumatoid Arthritis: A Bioinformatics-Based Exploration

Background Inflammatory bowel disease (IBD) is a chronic autoimmune-related disease that causes inflammation of the intestine. Rheumatoid arthritis (RA) can be as an extraintestinal complication occurring concurrently with IBD. However, the commonly dysregulated node of IBD and RA has not been studied. Methods We screened differentially expressed genes (DEGs) in the IBD and RA datasets from the Gene Expression Omnibus (GEO). Gene Ontology (GO) and Kyoto Encyclopedia of Genes and Genomes (KEGG) were used to enrichment analysis. Determined the significant hub genes by constructing protein-protein interaction (PPI) network. Further search for the transcription factors that regulate the hub genes, and verify the expression of the hub genes and the transcription factors in additional IBD and RA datasets. Finally, the transcription factor PAX5 was validated by multiplex immunohistochemistry (mIHC) in the tissues of IBD and RA. Results 54 consensus DEGs showed strong disease association. GO analysis indicated that these genes were significantly enriched for activation of immune response. KEGG analysis showed these genes may be involved in the cytokine-cytokine receptor inter-action. The PPI enrichment analysis identified 10 hub genes, and transcription factor PAX5 regulates CD19 and CD79A among these 10 hub genes. PAX5 was selected as the optimal common dysregulated node for IBD and RA. The result was confirmed by mIHC. Conclusion Our integrated analysis reveals PAX5 as a key molecular link between IBD and RA, functioning through B-cell regulation (CD19/CD79A) and serving as both a diagnostic marker and therapeutic target. These findings provide the first evidence of a shared pathogenic mechanism connecting gut-joint inflammation via PAX5-mediated immune dysregulation.