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The pathogenesis of viral-induced diabetes
Institution:1. Biochemistry, Biomedical Center (BMC), Ludwig-Maximilians University, Munich, Germany;2. Munich Cluster for Systems Neurology (SyNergy), Munich, Germany;3. Department of Molecular Genetics, Neurodegenerative Brain Diseases Group, VIB, Antwerp, Belgium;4. Laboratory of Neurogenetics, Institute Born-Bunge, University of Antwerp, Antwerp, Belgium;5. German Center for Neurodegenerative Diseases, DZNE, Munich, Germany;1. Children''s Hospital, Zhejiang University School of Medicine, Hangzhou 310052, China;2. Clinical Laboratory, Hangzhou First People''s Hospital, Hangzhou 310006, China;3. Institute of Immunology, Zhejiang University School of Medicine, Hangzhou 310058, China;1. State Key Laboratory of Microbial Technology, School of Life Sciences, Shandong University, Jinan, 250100, China;2. Genetic Disease Diagnosis Center, Zibo Maternal and Child Health Hospital, Affiliated to Shandong Academy of Medical Science, Zibo, Shandong, 255000, China;3. Medical Research & Laboratory Diagnostic Center, Jinan Central Hospital Affiliated to Shandong University, Jinan, China;4. Center for Gene and Immunotherapy, The Second Hospital of Shandong University, Jinan, 250012, China;2. Department of Cardiac Surgery, University of Michigan, Ann Arbor, MI;3. Banyan Biomarkers, Inc., Alachua, FL;4. Hugo Moser Research Institute at Kennedy Krieger and Departments of Neurology and Pediatrics, The Johns Hopkins University School of Medicine, Baltimore MD
Abstract:Serologic case-control studies have suggested an association between coxsasckie group B viruses and insulin-dependent diabetes mellitus (IDDM). New investigations have identified enteroviral nucleic acid in the peripheral blood mononuclear cells of newly-diagnosed patients with IDDM. The disease pathogenesis is dependent on several factors including the genetics of the host, strain of virus, activation status of autoreactive T-cells, upregulation of pancreatic MHC-1 antigens, molecular mimicry between viral and beta cell epitopes and direct islet cell destruction by viral cytolysis. Epitopes (IDDM-E1 and E2) on glutamate decarboxylase 65 (GAD65) are the most common targets for antibody and cellular-mediated autoimmune beta cell destruction.
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