Organ-specific autoimmunity frequently affects the endocrine system, including pancreatic islets. Type 1 diabetes mellitus (T1D) derives from the autoimmune destruction of insulin-secreting β-cells that is triggered by environmental factors (1, 2). Genetic predisposition accounts for 36–50% of disease susceptibility as demonstrated in monozygotic twin studies (3–5). Approximately 90% of new cases lack a family history of T1D indicating a large contribution of exogenous factors to pathogenesis. A variety of associations with viral infections have been reported for human diabetes including rubella, mumps, and cytomegalovirus. However, among investigated agents, human enteroviruses (HEVs) appear to play a prominent role (1).
Enteroviruses and causality of type 1 diabetes: how close we are?
BAJ, ANDREINASecondo
;MACCARI, GIUSEPPE;SALVATONI, ALESSANDROPenultimo
;TONIOLO, ANTONIOUltimo
2012-01-01
Abstract
Organ-specific autoimmunity frequently affects the endocrine system, including pancreatic islets. Type 1 diabetes mellitus (T1D) derives from the autoimmune destruction of insulin-secreting β-cells that is triggered by environmental factors (1, 2). Genetic predisposition accounts for 36–50% of disease susceptibility as demonstrated in monozygotic twin studies (3–5). Approximately 90% of new cases lack a family history of T1D indicating a large contribution of exogenous factors to pathogenesis. A variety of associations with viral infections have been reported for human diabetes including rubella, mumps, and cytomegalovirus. However, among investigated agents, human enteroviruses (HEVs) appear to play a prominent role (1).I documenti in IRIS sono protetti da copyright e tutti i diritti sono riservati, salvo diversa indicazione.