The Role of Bacterial Pathogens in Autoimmune Diseases: Breaking Self-Tolerance

Autoimmune diseases (ADs) arise when the immune system erroneously attacks self-tissues, often due to a breakdown in selftolerance. These conditions, influenced by genetic and environmental factors, are increasingly linked to bacterial infections as significant triggers. A healthy immune system protects the body against infections. However, when the immune system malfunctions, it attacks healthy cells, tissues, and organs of the body. This malfunction or dysfunction is called autoimmune disease and can affect any part of the body, impairing psychological function and potentially becoming fatal. This review explores how bacterial pathogens such as Helicobacter pylori, Campylobacter jejuni, and Mycobacterium tuberculosis contribute to autoimmunity through mechanisms like molecular mimicry, bystander activation, and epitope spreading. These processes provoke cross-reactive immune responses, amplify immune dysregulation, and exacerbate tissue damage. Epidemiological and experimental studies reveal strong associations between bacterial infections and diseases like Guillain-Barré syndrome, rheumatoid arthritis, and sarcoidosis. By analyzing the interactions between these pathogens and immune mechanisms, the review highlights the pivotal role of bacteria in disrupting immune tolerance and driving autoimmune disease progression. Moreover, therapeutic strategies such as antibiotics, immunomodulators, and vaccines targeting bacterial-induced autoimmunity offer promising avenues for prevention and treatment. Understanding the mechanisms of bacterial action provides valuable insights into the development of effective diagnostics, preventive measures, and therapies. This review emphasizes the need for continued research on bacterial pathogenesis in autoimmunity, particularly among genetically susceptible populations, to refine targeted clinical approaches and improve outcomes in these complex diseases.