Upregulation of adhesion molecules and class I HLA in the myocardium of chronic chagasic cardiomyopathy and heart allograft rejection, but not in dilated cardiomyopathy.
The immunohistochemical expression of adhesion molecules and class I HLA in chronic chagasic cardiomyopathy were compared with heart allograft rejection and dilated cardiomyopathy, to obtain new knowledge on the occurrence of autoimmunity and inflammation in the pathogenesis of chronic chagasic cardiomyopathy. Semiquantitative immunohistochemistry was performed for CD8+ T cells, ICAM-1, VCAM-1, LFA-1, and class I HLA in frozen sections of myocardial biopsies from patients presenting chronic chagasic cardiomyopathy (group I, n = 12), heart allograft rejection (group II, n = 9) or dilated cardiomyopathy (group III, n = 9). A high mean number of CD8+ T cells/mm(2) was present in group I (18.26) and group II (28.60), but not in group III (0.83). The frequency of high expression for ICAM-1 and VCAM-1 on the endothelial and interstitial cells, and for class I HLA on the cardiomyocytes was greater in group I (100%, 33.3%, and 83.3%, respectively) and group II (100%, 66.7%, and 77.8%, respectively), compared to group III (66.7%, 0%, and 0%, respectively). ICAM-1 and VCAM-1 probably participate in the development of the lymphocytic inflammatory infiltrate present in chronic chagasic cardiomyopathy, as seen in heart allograft rejection. The overexpression of adhesion molecules and the induction of class I HLA on the cardiomyocytes are probably related to the high cytokine levels at the inflammatory sites in chronic chagasic cardiomyopathy. Although the induction of class I HLA on the cardiomyocytes is consistent with an autoimmune reaction, it should not be considered as irrefutable evidence for autoimmunity in chronic chagasic cardiomyopathy. The differential expression of adhesion molecules and class I HLA in dilated cardiomyopathy compared to chronic chagasic cardiomyopathy suggests differences in the pathogenesis of these cardiomyopathies.
Benvenuti
L A
LA
Department of Pathology, Heart Institute (InCor), University of São Paulo Medical School, São Paulo, Brazil. anpluiz@incor.usp.br
Higuchi
M L
ML
Reis
M M
MM
D000328:Adult; D002311:Cardiomyopathy, Dilated / Q000378:metabolism; D015815:Cell Adhesion Molecules / Q000378:metabolism*; D002598:Chagas Cardiomyopathy / Q000378:metabolism*; D002908:Chronic Disease; D005260:Female; D006084:Graft Rejection / Q000378:metabolism*; D016027:Heart Transplantation; D015395:Histocompatibility Antigens Class I / Q000378:metabolism*; D006801:Humans; D007150:Immunohistochemistry; D008297:Male; D008875:Middle Aged; D009206:Myocardium / Q000378:metabolism*; D014184:Transplantation, Homologous; D015854:Up-Regulation
D015815:Cell Adhesion Molecules; D015395:Histocompatibility Antigens Class I