Endomyocardial HLA expression is increased to the same extent in idiopathic and secondary dilated cardiomyopathy

• Published in: Immunology letters Vol. 41; no. 1; pp. 59 - 66
• Main Authors: Klappacher, Günter, Mehrabi, Mohammad, Franzen, Patrick, Plesch, Karina, Binder, Michael, Haab, Doris, Urban, Susanne, Laufer, Günter, Dietmar Glogar, H., Eichler, Hans-Georg
• Format: Journal Article
• Language: English
• Published: Amsterdam Elsevier B.V 01.06.1994; Elsevier
• Subjects: Biological and medical sciences; Cardiology. Vascular system; Cardiomyopathy, Dilated - immunology; Cardiomyopathy, Hypertrophic - immunology; Chronic heart failure; Dilated cardiomyopathy; Endocardium - immunology; Female; Fibroblasts - immunology; Heart; Heart failure, cardiogenic pulmonary edema, cardiac enlargement; Heart Transplantation; HLA Antigens - biosynthesis; Humans; Immunoenzyme Techniques; Lymphocyte Activation; Major histocompatibility complex; Male; Medical sciences; Middle Aged; Myocardium - immunology; T-cell activation; T-Lymphocytes - immunology; Major histocompatibility complex; Chronic heart failure; Dilated cardiomyopathy; T-cell activation; Heart; Human; Heart failure; HLA-System; Cardiomyopathy; Heart disease; Major histocompatibility system; T-Lymphocyte; Cardiovascular disease; Activation; Transplantation; Myocardial disease
• ISSN: 0165-2478; 1879-0542
• DOI: 10.1016/0165-2478(94)90057-4

In a total of 22 failing hearts from human transplant recipients, the expression of major histocompatibility complex (MHC) molecules, the CD phenotype of infiltrating mononuclear cells, and the number of fibroblasts were analyzed by immunohistochemistry. Compared with 10 non-failing control hearts, significantly higher morphometric area fractions of HLA-ABC and HLA-DR with a concomitant increase of CD3-, CD4- and CD8-positive cells were found to be comparable in 12 patients with idiopathic dilated cardiomyopathy and in 10 patients with secondary heart failure. Furthermore, the similarity of T-cell activation in idiopathic and secondary variants of the disease were substantiated by the following observations: (1) the site-specific distribution of MHC molecules and mononuclear cells in the myocardium was comparable in idiopathic and secondary dilated cardiomyopathy; (2) 6 individuals with lymphocytic aggregates in their myocardium in association with the highest levels of HLA-ABC expression were equally distributed among idiopathic and secondary patient subsets; and (3) expression of HLA-ABC and HLA-DR correlated with that of an endothelial cell marker, von Willebrand factor, in failing myocardia of both study groups. In conclusion, no difference was found in increased MHC molecule expression in failing myocardium of idiopathic and secondary variants of dilated cardiomyopathy, and these entities were not differentially associated with infiltration by increased numbers of T lymphocytes. Hence, we postulate that these immunopathological features are consequences rather than causative factors of myocardial degeneration and dilatation. This view contrasts with the current concept that specific abnormalities of T cell-mediated immunity would reflect postinfectious autoimmunity and that this type of immune reaction was restricted to the idiopathic form of dilated cardiomyopathy.