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Viral infections in type 1 diabetes mellitus ? why the ? cells? #MMPMID27020257
de Beeck AO; Eizirik DL
Nat Rev Endocrinol 2016[May]; 12 (5): 263-73 PMID27020257show ga
Type 1 diabetes mellitus (T1DM) is caused by progressive autoimmune-mediated loss of pancreatic ?-cell mass via apoptosis. The onset of T1DM depends on environmental factors that interact with predisposing genes to induce an autoimmune assault against ? cells. Epidemiological, clinical and pathology studies in humans support viral infection ? particularly by enteroviruses (for example, coxsackievirus) ? as an environmental trigger for the development of T1DM. Many candidate genes for T1DM, such as MDA5, PTPN2 and TYK2, regulate antiviral responses in both ? cells and the immune system. Cellular permissiveness to viral infection is modulated by innate antiviral responses that vary among different tissues or cell types. Some data indicate that pancreatic islet ? cells trigger a more efficient antiviral response to infection with diabetogenic viruses than do ? cells, and so are able to eradicate viral infections without undergoing apoptosis. This difference could account for the varying ability of islet-cell subtypes to clear viral infections and explain why chronically infected pancreatic ? cells, but not ? cells, are targeted by an autoimmune response and killed during the development of T1DM. These issues and attempts to target viral infection as a preventive therapy for T1DM are discussed in the present Review.
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Nat+Rev+Endocrinol 2016 ; 12 (5): 263-73
