Cytotoxic T Lymphocytes Are Activated Following Myocardial Infarction and Can Recognize and Kill Healthy Myocytes In Vitro

Cytotoxic T Lymphocytes Are Activated Following Myocardial Infarction and Can Recognize and Kill Healthy Myocytes In Vitro

The damage of myocardial infarction (MI) is often progressive. A possible mechanism for subsequent myocardial damage and heart failure after MI is immune response against cardiac self-antigens. The purpose of our study was to test the hypothesis that cytotoxic T lymphocytes are activated following a...

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Bibliographic Details
Published in:Journal of molecular and cellular cardiology Vol. 32; no. 12; pp. 2141 - 2149
Main Authors: Varda-Bloom, Nira, Leor, Jonathan, Ohad, Dan G., Hasin, Yonathan, Amar, Merry, Fixler, Ruhama, Battler, Alexander, Eldar, Michael, Hasin, David
Format: Journal Article
Language:English
Published: England Elsevier Ltd 01-12-2000
Subjects:
Animals
Animals, Newborn
CD8-Positive T-Lymphocytes - metabolism
Cell Survival
Cells, Cultured
Coculture Techniques
Dose-Response Relationship, Drug
Inflammation
Lymphocyte Activation
Lymphocytes
Major Histocompatibility Complex
Male
Myocardial infarction
Myocardial Infarction - metabolism
Myocardial Infarction - pathology
Myocarditis
Myocardium - cytology
Myocardium - pathology
Rats
Rats, Sprague-Dawley
Rats, Wistar
Reperfusion
Spleen - cytology
T-Lymphocytes, Cytotoxic - metabolism
Thymidine - metabolism
Time Factors
Myocardial infarction
Myocarditis
Inflammation
Reperfusion
Lymphocytes
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Summary:The damage of myocardial infarction (MI) is often progressive. A possible mechanism for subsequent myocardial damage and heart failure after MI is immune response against cardiac self-antigens. The purpose of our study was to test the hypothesis that cytotoxic T lymphocytes are activated following acute MI and may have a role in producing further myocardial damage. Rats were allocated into three experimental groups: acute MI, Sham MI and non-operated control. One, two and three weeks after surgery, lymphocytes were obtained from rat spleens and incubated with neonatal cardiac myocytes. Lymphocyte proliferation was assessed by a thymidine incorporation assay and calculated as proliferation index (PI). Myocyte destruction was measured by a crystal–violet staining assay and expressed as percentage of cell destruction. Proliferation index was significantly higher among lymphocytes obtained from MI animals (44.3±5.8 and 44.9±5.1, at 2 and 3 weeks after MI, respectively) than sham MI (29.3±5.3, 27.1±4.7) (P<0.05) or control animals (17.1±2.5, 16.2±2.8) (P=0.03). Cytotoxic activity of the MI lymphocytes against the cultured cardiomyocytes was significantly higher 2 and 3 weeks after MI, (36.4±7.3%, 69.3±4.9%) compared to sham MI (17.9±3.14%, 36.6±5.3%) (P<0.001) and control animals respectively (13.3±5.4%, 17.4±6.1%) (P<0.001). The cytotoxic activity against healthy cardiomyocytes was myocyte-specific, induced by CD8 lymphocytes and major-histocompatibility complex (MHC) restricted. Cytotoxic T lymphocytes (CD8) are activated following MI and can recognize and kill normal cardiomyocytes in vitro. The newly described pathophysiological insights may provide novel oportunities to prevent death of non-ischemic cardiomyocytes and heart failure following myocardial infarction.
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ISSN:0022-2828
1095-8584
DOI:10.1006/jmcc.2000.1261