Type 1 diabetes mellitus is a chronic autoimmune disease resulting from the progressive immune-mediated destruction of pancreatic beta cells in genetically susceptible individuals, with the likely contribution of environmental factors, among which viruses have been extensively studied. The pathologic hallmark of the disease is insulitis-a process characterized by islet infiltration of immunocompetent cells that has been well characterized in animal models of islet autoimmunity, and to a lesser extent, in humans. Insulitis characterization has provided valuable information to gain insights into the disease pathogenesis. We review the recent literature on the viral contribution to beta-cell destruction and dysfunction in type 1 diabetes, with particular reference to the pathology of the pancreatic islet in humans and in animal models of the disease.

Dotta, F., Galleri, L., Sebastiani, G., & Vendrame, F. (2010). Virus infections: lessons from pancreas histology. CURRENT DIABETES REPORT, 10(5), 357-361 [10.1007/s11892-010-0137-z].

Virus infections: lessons from pancreas histology.

DOTTA, FRANCESCO;SEBASTIANI G.;
2010

Abstract

Type 1 diabetes mellitus is a chronic autoimmune disease resulting from the progressive immune-mediated destruction of pancreatic beta cells in genetically susceptible individuals, with the likely contribution of environmental factors, among which viruses have been extensively studied. The pathologic hallmark of the disease is insulitis-a process characterized by islet infiltration of immunocompetent cells that has been well characterized in animal models of islet autoimmunity, and to a lesser extent, in humans. Insulitis characterization has provided valuable information to gain insights into the disease pathogenesis. We review the recent literature on the viral contribution to beta-cell destruction and dysfunction in type 1 diabetes, with particular reference to the pathology of the pancreatic islet in humans and in animal models of the disease.
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Utilizza questo identificativo per citare o creare un link a questo documento: http://hdl.handle.net/11365/10783
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