Abstract

Type 1 diabetes (T1D) results from genetic predisposition and environmental factors leading to the autoimmune destruction of pancreatic beta cells. Recently, a rapid increase in the incidence of childhood T1D has been observed worldwide; this is too fast to be explained by genetic factors alone, pointing to the spreading of environmental factors linked to the disease. Enteroviruses (EVs) are perhaps the most investigated environmental agents in relationship to the pathogenesis of T1D. While several studies point to the likelihood of such correlation, epidemiological evidence in its support is inconclusive or in some instances even against it. Hence, it is still unknown if and how EVs are involved in the development of T1D. Here we review recent findings concerning the biology of EV in beta cells and the potential implications of this knowledge for the understanding of beta cell dysfunction and autoimmune destruction in T1D.

Highlights

  • In type 1 diabetes (T1D), the insulin-producing pancreatic beta cells are destroyed by misguided immune cells

  • More than 40 genetic loci associated with T1D have been identified including those of insulin, cytotoxic T lymphocyte antigen 4 (CTLA-4), interleukin 2 receptor a (IL2RA), tyrosine phosphatase PTPN22, and the viral double-stranded RNA sensor IFIH1 [3]

  • These data point to the contribution of environmental factors toward the onset and/or progression of autoimmunity directed against beta cells

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Summary

Introduction

In type 1 diabetes (T1D), the insulin-producing pancreatic beta cells are destroyed by misguided immune cells. Genetic as well as environmental factors affecting the immune system and possibly beta cells contribute to the development of the disease. Migration studies have shown that children of immigrants, who moved from an area with a low incidence to an area of high incidence of T1D, increased their risk for developing the disease compared to children in the area of origin [8, 9]. Taken together, these data point to the contribution of environmental factors toward the onset and/or progression of autoimmunity directed against beta cells

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Conclusions
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