Catecholamines induce IL-10 release in patients suffering from acute myocardial infarction by transactivating its promoter in monocytic but not in T-cells

2000 ◽  
pp. 45-50 ◽  
Author(s):  
Ulrike Riese ◽  
Susanne Brenner ◽  
Wolf-Dietrich Döcke ◽  
Susanna Prösch ◽  
Petra Reinke ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells

scholarly journals Peripheral Levels of EPCs, T Cells, and Macrophages’ as Possible Predictive Biomarkers of Acute Myocardial Infarction

2020 ◽  
Author(s):  
Amankeldi Salybekov ◽  
Katsuaki Sakai ◽  
Makoto Natsumeda ◽  
Kosit Vorateera ◽  
Shuzo Kobayashi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
Cd8 T Cells ◽  
Immune Cell ◽  
Temporal Dynamics ◽  
Predictive Biomarkers ◽  
Mortality And Morbidity ◽  
Patients With Diabetes ◽  
Functionally Impaired

Abstract Acute myocardial infarction (AMI), with a very relevant global disease burden, remains the major mortality and morbidity cause among all cardiovascular diseases. Patient prognosis is strictly dependent on early diagnosis and the adoption of adequate interventions. AMI diagnosis requires constant optimization, particularly considering the individuals at higher risk (or more vulnerable to worse outcomes) such as patients with diabetes mellitus and atherosclerosis. Herein, we investigated the levels of peripheral blood EPCs and immune cell-subsets from myeloid and lymphoid lineages, as well as their temporal dynamics, in the quest for new prognostic biomarkers of AMI. We collected blood from 18 hospitalized patients (days 3 and 7 after AMI onset) and 16 healthy volunteers, and resolved their circulating PBMC populations via flow cytometry. Overall, our data demonstrate a significant decrease in peripheral EPCs and CD8+ T cells, three days following an AMI. EPCs appear to be functionally impaired in AMI patients, and their circulating numbers associate with cardiac vessel lesions. Furthermore, CD8+ T cells (and even M1-macrophages) in the periphery, in combination with the classical laboratory determinations, may serve as high accuracy biomarkers of AMI, potentially aiding to prevent worse AMI outcomes.

Potential role of invariant natural killer T cells in outcomes of acute myocardial infarction

2015 ◽  
Vol 187 ◽  
pp. 663-665 ◽  
Author(s):  
Jan Novak ◽  
Jan Dobrovolny ◽  
Petr Tousek ◽  
Viktor Kocka ◽  
Elena Teringova ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
Natural Killer ◽  
Potential Role ◽  
Natural Killer T Cells ◽  
Killer T Cells ◽  
Invariant Natural Killer ◽  
Natural Killer T

Recruitment of circulating dendritic cell precursors into the infarcted myocardium and pro-inflammatory response in acute myocardial infarction

2012 ◽  
Vol 123 (6) ◽  
pp. 387-398 ◽  
Author(s):  
Daniel Kretzschmar ◽  
Stefan Betge ◽  
Alexander Windisch ◽  
Rudin Pistulli ◽  
Ilonka Rohm ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
Dendritic Cells ◽  
Dendritic Cell ◽  
Interleukin 2 ◽  
Serum Levels ◽  
Myeloid Dendritic Cells ◽  
Peripheral Tissues ◽  
Infarcted Myocardium

DC (dendritic cells) play an important role in the immune system. They invade peripheral tissues to detect harmful antigens, inducing a local immune response. Studies suggest that DCPs (dendritic cell precursors) might be reduced in AMI (acute myocardial infarction); however, the reason for their reduction is unknown yet. In the present study, circulating mDCPs (myeloid DCPs), pDCPs (plasmacytoid DCPs), tDCPs (total DCPs) and serum levels of TNFα (tumour necrosis factor α), IL (interleukin)-2, -4, -5, -6, -10 and -12 were analysed by flow cytometry in blood of patients with NSTEMI [non-STEMI (ST-segment elevation myocardial infarction)] (n=44) and STEMI (n=34) compared with controls with excluded CAD (coronary artery disease) (n=45). Post-mortem myocardial specimens of patients with AMI (n=12) and healthy myocardium of accident victims (n=10) were immunostained for mDCs (myeloid dendritic cells) T-cells and macrophages. Compared with controls, in patients with AMI a significant decrease in circulating mDCPs, pDCPs and tDCPs was observed (each P<0.0001). The extent of the decrease was higher in STEMI than NSTEMI patients. Serum levels were significantly higher in patients with AMI compared with controls for IL-6, -10, -12 and TNFα (each P<0.03). Immunostaining revealed significantly higher number of DCs, T-cells and macrophages (each P<0.002) in infarcted than control myocardium. We show that circulating DCPs are significantly reduced in AMI, with a pronounced reduction in STEMI patients. This was accompanied by a significant increase of inflammatory serum cytokines in patients with AMI. Immunohistochemical analysis unravelled that the reduction of circulating DCPs might be due to recruitment into the infarcted myocardium.

CD8+CD28+ T cells might mediate injury of cardiomyocytes in acute myocardial infarction

2018 ◽  
Vol 101 ◽  
pp. 74-79 ◽  
Author(s):  
Lili Zhang ◽  
Zhiyan Wang ◽  
Di Wang ◽  
Jumo Zhu ◽  
Yi Wang
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells

Exosomes derived from regulatory T cells ameliorate acute myocardial infarction by promoting macrophage M2 polarization

IUBMB Life ◽  
2020 ◽  
Vol 72 (11) ◽  
pp. 2409-2419
Author(s):  
Hao Hu ◽  
Jiawei Wu ◽  
Cheng Cao ◽  
Likun Ma
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
Regulatory T Cells ◽  
M2 Polarization

scholarly journals CD100 modulates cytotoxicity of CD8+ T cells in patients with acute myocardial infarction

2021 ◽  
Vol 22 (1) ◽  
Author(s):  
Yan Li ◽  
Li Qin ◽  
Qijun Bai ◽  
Jingjing Zhang ◽  
Ruixue Chen ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
T Cell ◽  
Angina Pectoris ◽  
Cell Activity ◽  
Regulatory Function ◽  
Indirect Contact ◽  
Direct Cytotoxicity ◽  
Membrane Bound

Abstract Background 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. Methods Peripheral 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. Results AMI 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. Conclusion Up-regulation of MMP-2 might contribute to elevation of mCD100 shedding and sCD100 formation, leading to increased cytotoxicity CD8+ T cells in AMI patients.

scholarly journals Cytotoxic CD8+ T cells promote granzyme B-dependent adverse post-ischemic cardiac remodeling

2021 ◽  
Vol 12 (1) ◽  
Author(s):  
Icia Santos-Zas ◽  
Jeremie Lemarié ◽  
Ivana Zlatanova ◽  
Marine Cachanado ◽  
Jean-Christophe Seghezzi ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
T Cells ◽  
T Lymphocytes ◽  
Heart Function ◽  
Ischemia Reperfusion ◽  
Granzyme B ◽  
Acute Ischemia ◽  
Risk Of Death ◽  
Increased Risk

AbstractAcute myocardial infarction is a common condition responsible for heart failure and sudden death. Here, we show that following acute myocardial infarction in mice, CD8+ T lymphocytes are recruited and activated in the ischemic heart tissue and release Granzyme B, leading to cardiomyocyte apoptosis, adverse ventricular remodeling and deterioration of myocardial function. Depletion of CD8+ T lymphocytes decreases apoptosis within the ischemic myocardium, hampers inflammatory response, limits myocardial injury and improves heart function. These effects are recapitulated in mice with Granzyme B-deficient CD8+ T cells. The protective effect of CD8 depletion on heart function is confirmed by using a model of ischemia/reperfusion in pigs. Finally, we reveal that elevated circulating levels of GRANZYME B in patients with acute myocardial infarction predict increased risk of death at 1-year follow-up. Our work unravels a deleterious role of CD8+ T lymphocytes following acute ischemia, and suggests potential therapeutic strategies targeting pathogenic CD8+ T lymphocytes in the setting of acute myocardial infarction.

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