Unravelling the mechanistic link between enterovirus infection and type 1 diabetes



One of the reasons researchers are struggling to develop novel treatments for T1D is that the mechanisms underlying the development of disease are not fully understood. A long-standing dogma is that pancreatic β-cells (which produce the hormone insulin to maintain glucose homeostasis) are destroyed by the immune system in response to environmental influence resulting in insulin-deficiency and hyperglycemia. Enteroviruses are the potential environmental triggers of T1D that have been subjected to the most intense scrutiny at present, with over 700 publications on enterovirus and T1D in PubMed. We have demonstrated that infection with particular members of the enterovirus genus (i.e. echoviruses 4, echovirus 16, and echovirus 30) led to some individuals developing diabetes-related autoantibodies (i.e. islet cell antibodies [ICA], insulin autoantibodies [IAA], glutamic acid decarboxylase antibodies [GADA]). These strains were able to replicate in human primary pancreatic islets and β-cell-derived lines (i.e. INS-1 832/13, MIN6, and NIT-1 cells). Importantly, we have recently demonstrated that certain enterovirus strains (i.e. E6) can replicate in human pancreatic exocrine cells. These findings support the view that enteroviruses are able to target both pancreatic exocrine and endocrine cells and trigger islet autoimmunity.
StatusEj startat