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Titlebook: Autoimmunity and the Pathogenesis of Diabetes; Fredda Ginsberg-Fellner (Professor of Pediatrics, Book 1990 Springer-Verlag New York Inc.

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Immune Intervention in Diabetes: State of the Art and Future Directions,s depends on three main lines of evidence. First the association of IDDM with markers of the major histocompatibility complex (MHC) indicates not only that genetic factors are important in determining susceptibility to the disease but also that this may be related to immune system functions.. Second
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,Diskursanalyse literarischer Geständnisse,c susceptibility. Triggering factors that might induce diabetes include diabetogenic viruses, chemicals, diet, and toxins. Such likely candidates act either as primary injurious agents to pancreatic beta-cells or as triggers of autoimmunity in man and animals (Fig. 10.1)..
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Damian M. Lyons,Daniel L. Pelletierted. Do autoantibodies appear after presentation of islet antigens as the primary event? Do they appear following an undefined injury to beta-cells? The latter may include attacks by virus, bacteria, environmental antigens, or possible cytotoxic lymphocytes that have been activated to detect beta-cell antigens.
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Michael Blatz,Karl-J. Kraus,Sascha Haghani transplantation in discordant identical twins, during which the histology of the pancreatitis that occurs in the recipient in the absence of immunosuppression has been studied.. Investigations concerning each of these lines of evidence continue, as discussed elsewhere in this volume.
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The Humoral Anti-Islet Immune Response: Cytoplasmic Islet-Cell Antibodies: Technical Aspects and Clogressive destruction of the insulin-producing beta-cells of the islets of Langerhans; unequivocal proof for a direct autoimmune attack against beta-cells has yet to be demonstrated, however, despite the finding of a constellation of immune abnormalities around and inside injured islets at the time of diagnosis..
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Immune Intervention in Diabetes: State of the Art and Future Directions, transplantation in discordant identical twins, during which the histology of the pancreatitis that occurs in the recipient in the absence of immunosuppression has been studied.. Investigations concerning each of these lines of evidence continue, as discussed elsewhere in this volume.
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