NDLI: Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.

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Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.

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Autoimmune cardiomyopathy and heart block develop spontaneously in HLA-DQ8 transgenic IAbeta knockout NOD mice.

Content Provider	World Health Organization (WHO)-Global Index Medicus
Author	Liu, Gang Rayner, David Bautista-lopez, Norma Suzuki, Kunimasa Elliott, John F. Nation, Patrick Kavanagh, Katherine M. Liu, Junliang Yuan, Zuan-ning Robertson, Murray A. Wallbank, Sarah L.
Description	Author Affiliation: Elliott JF ( Department of Medical Microbiology and Immunology, University of Alberta, Edmonton, AB, Canada T6G 2S2. john.elliott@ualberta.ca);
Abstract	A line of nonobese diabetic (NOD) mice expressing the human diabetes-associated HLA-DQ8 transgene in the absence of mouse IAbeta failed to show spontaneous insulitis or diabetes, but rather developed dilated cardiomyopathy, leading to early death from heart failure. Pathology in these animals results from an organ- and cell-specific autoimmune response against normal cardiomyoctes in the atrial and ventricular walls, as well as against very similar myocytes present in the outermost muscle layer surrounding the pulmonary veins. Progression of the autoimmune process could be followed by serial ECG measurements; irradiation of young animals significantly delayed disease progression, and this effect could be reversed by adoptive transfer of splenocytes taken from older animals with complete heart block. Disease progression could also be blocked by cyclosporin A treatment, but was accelerated by injection of complete Fruend's adjuvant. The constellation of findings of spontaneously arising destructive focal lymphocytic infiltrates within the myocardium, rising titers of circulating anticardiac autoantibodies, dilation of the cardiac chambers, and gradual progression to end-stage heart failure bears a striking resemblance to what is seen in humans with idiopathic dilated cardiomyopathy, a serious and often life-threatening medical condition. This transgenic strain provides a highly relevant animal model for human autoimmune myocarditis and postinflammatory dilated cardiomyopathy.
ISSN	00278424
e-ISSN	10916490
Journal	Proceedings of the National Academy of Sciences of the United States of America
Issue Number	23
Volume Number	100
Language	English
Publisher	National Academy of Sciences
Publisher Date	2003-11-01
Publisher Place	United States
Access Restriction	Open
Subject Keyword	Autoimmune Diseases Genetics Cardiomyopathies HLA-DQ Antigens Heart Block Animals Blotting, Western Cell Division Cyclosporine Pharmacology Disease Progression Electrocardiography Enzyme-Linked Immunosorbent Assay Freund's Adjuvant Immunohistochemistry Mice Mice, Inbred NOD Mice, Knockout Mice, Transgenic Myocardium Metabolism Spleen Cytology T-Lymphocytes Time Factors Research Support, Non-U.S. Gov't Multidisciplinary
Content Type	Text
Resource Type	Article
Subject	Multidisciplinary

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