作者: Isabella Spagnuolo , Aurora Patti , Guido Sebastiani , Laura Nigi , Francesco Dotta
DOI: 10.1097/MED.0B013E328362A7D7
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摘要: PURPOSE OF REVIEW Type 1 diabetes (T1D) results from the immune-mediated destruction of pancreatic insulin-producing cells because interaction among genetic susceptibility, immune system and environmental factor(s). A possible role viral infections in T1D pathogenesis has been hypothesized for some time; however, only most recent years, studies performed at molecular cellular level are starting to shed light on this issue. RECENT FINDINGS Studies animal models man have shown that viruses can indeed infect beta-cells, inducing islet inflammation functional damage. In addition, in-situ investigations tissue samples provided evidence addition adaptive response, innate immunity is involved whole pancreas (not its endocrine portion) infiltrated by phenomena. SUMMARY The established insulitic process increasing support contribution a proinflammatory scenario strongly suggestive may contribute beta-cell damage dysfunction, thus setting stage design antiviral strategies (e.g. vaccines drugs) aimed protecting beta-cells.