Identification of common genetic factors and immune-related pathways associating more than two autoimmune disorders: implications on risk, diagnosis, and treatment

Abstract

Autoimmune disorders (ADs) are chronic conditions resulting from failure or breakdown of immunological tolerance, resulting in the host immune system attacking its cells or tissues. Recent studies report shared effects, mechanisms, and evolutionary origins among ADs; however, the possible factors connecting them are unknown. This study attempts to identify gene signatures commonly shared between different autoimmune disorders and elucidate their molecular pathways linking the pathogenesis of these ADs using an integrated gene expression approach. We employed differential gene expression analysis across 19 datasets of whole blood/peripheral blood cell samples with five different autoimmune disorders (rheumatoid arthritis, multiple sclerosis, systemic lupus erythematosus, Crohn’s disease, and type 1 diabetes) to get nine key genes—EGR1, RUNX3, SMAD7, NAMPT, S100A9, S100A8, CYBB, GATA2, and MCEMP1 that were primarily involved in cell and leukocyte activation, leukocyte mediated immunity, IL-17, AGE-RAGE signaling in diabetic complications, prion disease, and NOD-like receptor signaling confirming its role in immune-related pathways. Combined with biological interpretations such as gene ontology (GO), pathway enrichment, and protein–protein interaction (PPI) network, our current study sheds light on the in-depth research on early detection, diagnosis, and prognosis of different ADs.

Supplementary Information

The online version contains supplementary material available at 10.1186/s44342-024-00004-5.