المؤلفون: Grieco, Fabio Arturo^1,2, Vendrame, Francesco³, Spagnuolo, Isabella^1,2, Dotta, Francesco^1,2,4

المصدر: Seminars in Immunopathology. Mar2011, Vol. 33 Issue 1, p57-66. 10p. 1 Color Photograph, 2 Diagrams, 1 Chart.

مصطلحات موضوعية: *DIABETES, *IMMUNOLOGY, *TUMOR necrosis factors, *RNA, *ANTIGENS, *KILLER cells, *AUTOIMMUNE diseases, *PROINSULIN

مستخلص: Type 1 diabetes mellitus is an autoimmune disease caused by the immune-mediated destruction of insulin-producing pancreatic beta cells occurring in genetically predisposed individuals, with consequent hyperglycemia and serious chronic complications. Studies in man and in experimental animal models have shown that both innate and adaptive immune responses participate to disease pathogenesis, possibly reflecting the multifactorial pathogenetic nature of this autoimmune disorder, with the likely involvement of environmental factors occurring at least in a subset of individuals. As a consequence, components of both innate and adaptive immune response should be considered as potential targets of therapeutic strategies for disease prevention and cure. Here we review the contribution of innate immune response to type 1 diabetes, with a particular emphasis to Toll-like receptors (TLR) and NK cells. [ABSTRACT FROM AUTHOR]

المؤلفون: Dotta, Francesco, Galleri, Letizia, Sebastiani, Guido, Vendrame, Francesco

المصدر: Current Diabetes Reports; Oct2010, Vol. 10 Issue 5, p357-361, 5p

مستخلص: Type 1 diabetes mellitus is a chronic autoimmune disease resulting from the progressive immune-mediated destruction of pancreatic β 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 β-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. [ABSTRACT FROM AUTHOR]

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