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Helicobacter pylori (H. pylori) is a spiral-shaped, gram-negative, flagellated bacteria that causes gastritis symptoms. This bacterium, particularly in individuals with a genetic predisposition, has been implicated in the pathogenesis of several autoimmune diseases (AD) through complex mechanisms involving the interaction of cellular and humoral immune responses. This review article tells you about the link between H. pylori infection and several types of AD, including systemic lupus erythematosus (SLE), autoimmune pancreatitis (AIP), rheumatoid arthritis (RA), Sjögren syndrome (SjS), psoriasis, and antiphospholipid syndrome (APS). We conducted a comprehensive analysis of the current literature to elucidate the potential role of H. pylori as a triggering factor for these disorders. Our findings suggest a significant correlation between H. pylori infection and the onset or exacerbation of specific ADs. This relationship is common mechanisms, including molecular mimicry, chronic inflammation, epitope spreading, and cytokine dysregulation. While H. pylori is implicated in AD, other factors such as genetic predisposition, environmental triggers, and other microbial agents also play crucial roles. Other pathogens, such as Epstein-Barr virus (EBV), cytomegalovirus (CMV), and bacteria like Mycobacterium tuberculosis and Chlamydia pneumoniae have been linked to ADs. These shared pathways highlight the potential role of H. pylori as a unifying factor in the pathogenesis of diverse ADs. Further research is necessary to fully understand the interactions between H. pylori and the immune system in the context of autoimmunity. This review aims to provide a detailed overview of the knowledge on this topic, highlighting the need for additional studies to clarify these complex relationships.
Yarahmadi et al. (Fri,) studied this question.
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