01 March 2005 : Case report
Med Sci Monit 2005; 11(3): RA63-69 :: ID: 15398
Type 1 diabetes mellitus (T1DM) results from environmental factors acting on genetically susceptible individuals. Microbial infections and their immunological consequences are suspected to take part in the pathogenesis of T1DM. Congenital rubella infection has been strongly associated with increased disease susceptibility. In addition, infections with different strains of enteroviruses, human cytomegalovirus, and rotavirus have been suggested to be diabetogenic in susceptible individuals. A newly emerged hypothesis states that a bacterial toxin, bafilomycin A1 produced by Streptomyces spp, could be the cause of pancreatic beta-cell damage. In some instances, microbial infections may even protect the individual from T1DM. There are several proposed mechanisms of beta-cell damage caused by microbes. T1DM can result from direct cytolysis of beta-cells. Other suggested mechanisms are cross-reactivity between microbial proteins and self antigens (molecular mimicry), bystander activation of lymphocytes, and alterations in cytokine concentrations affecting T-helper cell balance in the vicinity of pancreatic beta-cells. Proving a causal role between microbial infections and T1DM appears difficult. Despite intensive research, a final conclusion concerning the causal role of microbes in the pathogenesis of T1DM has not been made.
Keywords: Diabetes Mellitus, Experimental - immunology, Diabetes Mellitus, Type 1 - etiology, Diabetes Mellitus, Type 1 - immunology, Diabetes Mellitus, Type 1 - microbiology, Diabetes Mellitus, Type 1 - virology, Enterovirus Infections - immunology, Islets of Langerhans - microbiology, Islets of Langerhans - pathology, Bacteria - pathogenicity, Bacterial Infections - immunology, Diabetes Mellitus, Experimental - immunology, Diabetes Mellitus, Type 1 - virology, Enterovirus Infections - immunology, Islets of Langerhans - pathology, Models, Biological, Molecular Mimicry - immunology, Rotavirus Infections - immunology, Rubella - immunology, T-Lymphocytes, Helper-Inducer - immunology, Virus Diseases - complications
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