Abstract
BackgroundCD100 is an immune semaphorin family member that highly expressed on T cells, which take part in the development of acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) are important mediators for membrane-bound CD100 (mCD100) shedding from T cells to generate soluble CD100 (sCD100), which has immunoregulatory effect on T cells. The aim of this study was to investigate modulatory role of CD100 on CD8+ T cell activity in AMI patients.MethodsPeripheral sCD100 and MMP-2 level, as well as mCD100 level on T cells was assessed in patients with stable angina pectoris (SAP), unstable angina pectoris (UAP), and AMI. The regulatory function of MMP-2 on mCD100 shedding, sCD100 formation, and cytotoxicity of CD8+ T cells was analyzed in direct and indirect contact co-culture system.ResultsAMI patients had higher peripheral sCD100 and lower mCD100 expression on CD8+ T cells in comparison with SAP, UAP, and controls. CD8+ T cells in AMI patients showed elevated direct cytotoxicity, enhanced cytokine production, and increased perforin/granzyme B secretion. Recombinant sCD100 stimulation promoted cytolytic function of CD8+ T cells in controls and AMI patients. Furthermore, AMI patients also had elevated circulating MMP-2 level. Recombinant MMP-2 stimulation induced mCD100 shedding from CD8+ T cells and sCD100 generation, resulting in enhancement of CD8+ T cell cytotoxicity in AMI patients.ConclusionUp-regulation of MMP-2 might contribute to elevation of mCD100 shedding and sCD100 formation, leading to increased cytotoxicity CD8+ T cells in AMI patients.
Highlights
CD100 is an immune semaphorin family member that highly expressed on T cells, which take part in the development of acute myocardial infarction (AMI)
Plasma soluble CD100 (sCD100) and Matrix metalloproteinase (MMP)-2 level was up-regulated in AMI patients sCD100 level was increased in AMI group (119.7 ± 18.67 ng/ml) compared with control group (99.34 ± 13.25 ng/ ml), stable angina pectoris (SAP) group (96.78 ± 8.59 ng/ml), and unstable angina pectoris (UAP) group (102.4 ± 13.71 ng/ml) (P < 0.01, Fig. 1a)
Plasma MMP-2 level was up-regulated in AMI group (310.7 ± 44.32 ng/ml) in comparison with control group (230.9 ± 64.46 ng/ml), SAP group (264.2 ± 69.54 ng/ml), and UAP group (240.7 ± 57.96 ng/ml) (P < 0.05, Fig. 1b)
Summary
CD100 is an immune semaphorin family member that highly expressed on T cells, which take part in the development of acute myocardial infarction (AMI). Matrix metalloproteinases (MMPs) are important mediators for membrane-bound CD100 (mCD100) shedding from T cells to generate soluble CD100 (sCD100), which has immunoregulatory effect on T cells. The aim of this study was to investigate modulatory role of CD100 on CD8+ T cell activity in AMI patients. Two forms of CD100 could be found as a membrane-bound dimer (mCD100) or as a soluble molecule (sCD100) originated via proteolytic cleavage by certain factors, especially matrix metalloproteinases (MMPs) [14, 15]. Regulation of CD100 expression and the role of CD100 to cytotoxicity of CD8+ T cells were not fully elucidated in coronary artery diseases
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