Cytotoxic lymphocytes and cardiac electrophysiology.
It is widely recognized that immune effector mechanisms contribute to cardiac dysfunction in major cardiac pathologies, such as myocarditis and the consequent dilated cardiomyopathy, Chagas' disease and heart transplant rejection. Of the wealth of immune mechanisms known to affect cardiac function, this review will deal with the adverse effects caused by cytotoxic T lymphocytes (CTL, CD4(+) and CD8(+) T lymphocytes), which participate in a broad range of heart pathologies. The interaction between cytotoxic lymphocytes and their target cells can set off two different effector mechanisms: (1) The perforin/granzymes, and (2) The Fas/FasL. In this review, I will discuss these mechanisms, and present experimental evidence showing that both can adversely affect cardiac myocytes in vitro, in a way that can contribute to a decline in the overall cardiac function.
Binah
Ofer
O
Rappaport Family Institute for Research in the Medical Sciences, Bruce Rappaport Faculty of Medicine, The Bernard Katz Minerva Center for Cell Biophysics, Technion-Israel Institute of Technology, Haifa, 31096, Israel. binah@tx.technion.ac.il
D000200:Action Potentials / Q000276:immunology / Q000502:physiology; D000818:Animals; D004594:Electrophysiology; D053222:Fas Ligand Protein; D006801:Humans; D015544:Inositol 1,4,5-Trisphosphate / Q000378:metabolism; D008562:Membrane Glycoproteins / Q000378:metabolism; D051379:Mice; D018448:Models, Immunological; D032383:Myocytes, Cardiac / Q000378:metabolism / Q000502:physiology*; D054353:Perforin; D052899:Pore Forming Cytotoxic Proteins; D013602:T-Lymphocytes, Cytotoxic / Q000276:immunology* / Q000378:metabolism; D019014:fas Receptor / Q000276:immunology / Q000378:metabolism
C505661:FASLG protein, human; D053222:Fas Ligand Protein; C505658:Fasl protein, mouse; D008562:Membrane Glycoproteins; D052899:Pore Forming Cytotoxic Proteins; D019014:fas Receptor; D054353:Perforin; D015544:Inositol 1,4,5-Trisphosphate