Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response...Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction （AMI）, Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes （such as death, recurrent myocardial in- farction, and heart failure） in patients with AMI.展开更多
AIM: To study the levels of T lymphocyte subsets andmembrane interleukin-2 receptor (mIL-2R) on surface ofperipheral blood mononuclear cells (PBMCs) of patients withhepatitis B and its role in the pathogenesis of hepa...AIM: To study the levels of T lymphocyte subsets andmembrane interleukin-2 receptor (mIL-2R) on surface ofperipheral blood mononuclear cells (PBMCs) of patients withhepatitis B and its role in the pathogenesis of hepatitis B.METHODS: The levels of T lymphocyte subsets and mIL-2R in PBMC before and after being stimulated with PHAwere detected by biotin-streptavidin (BSA) technique in 196cases of hepatitis B.RESULTS: In patients with hepatitis B, the levels of CD3+,CD4+ cells, and the ratio of CD4+ cells/CD8+ cells were lower,but the level of CD8+ cells was higher than those in normalcontrols (42.20±6.01 vs65.96±6.54, 38.17±5.93 vs41.73±6.40,0.91±0.28 vs 1.44±0.31, 39.86±6.36 vs30.02±-4.54, P＜0.01).The total expression level of mIL-2R in PBMC before andafter being stimulated with PHA was also lower than thosein normal controls (3.47±1.55 vs4.52±1.49, 34.03±2.94 vs37.95±3.00, P＜0.01). In all the patients with hepatitis B, thelevels of T lymphocyte subsets and mIL-2R in PBMC withHBV-DNA (+) were lower than those with HBV-DNA (-),which were significantly different (39.57±7.11 vs44.36±5.43,34.36±7.16 vs 40.75±5.87, 37.82±6.54 vs 41.72±6.21,0.88±0.33 vs0.99±0.27, 2.82±1.62 vs3.85±1.47, 31.56±3.00vs35.84±2.83, P＜0.01). In addition, the levels of CD3+, CD4+,CD8+ cells, the ratio of CD4+ cells/CD8+ cells and mIL-2R amongdifferent courses of hepatitis B were all significantly different(F=3 723.18, P＜0.01. F=130.43, P＜0.01. F=54.01, P＜0.01.F=2.99, P＜0.05. F=7.16, P＜0.01).CONCLUSION: Both cellular and humoral immune functionsare obviously in disorder in patients with hepatitis B, whichmight be closely associated with the chronicity in patients.展开更多
文摘Acute cardiomyocyte necrosis in the infarcted heart generates damage-associated molecular patterns, activating complement and toll-like receptor/interleukin-1 signaling, and triggering an intense inflammatory response. Iuflammasomes also recognize danger signals and mediate sterile inflammatory response following acute myocardial infarction （AMI）, Inflammatory response serves to repair the heart, but excessive inflammation leads to adverse left ventricular remodeling and heart failure. In addition to local inflammation, profound systemic inflammation response has been documented in patients with AMI, which includes elevation of circulating inflammatory cytokines, chemokines and cell adhesion molecules, and activation of peripheral leukocytes and platelets. The excessive inflammatory response could be caused by a deregulated immune system. AMI is also associated with bone marrow activation and spleen monocytopoiesis, which sustains a continuous supply of monocytes at the site of inflammation. Accumulating evidence has shown that systemic inflammation aggravates atherosclerosis and markers for systemic inflammation are predictors of adverse clinical outcomes （such as death, recurrent myocardial in- farction, and heart failure） in patients with AMI.
文摘AIM: To study the levels of T lymphocyte subsets andmembrane interleukin-2 receptor (mIL-2R) on surface ofperipheral blood mononuclear cells (PBMCs) of patients withhepatitis B and its role in the pathogenesis of hepatitis B.METHODS: The levels of T lymphocyte subsets and mIL-2R in PBMC before and after being stimulated with PHAwere detected by biotin-streptavidin (BSA) technique in 196cases of hepatitis B.RESULTS: In patients with hepatitis B, the levels of CD3+,CD4+ cells, and the ratio of CD4+ cells/CD8+ cells were lower,but the level of CD8+ cells was higher than those in normalcontrols (42.20±6.01 vs65.96±6.54, 38.17±5.93 vs41.73±6.40,0.91±0.28 vs 1.44±0.31, 39.86±6.36 vs30.02±-4.54, P＜0.01).The total expression level of mIL-2R in PBMC before andafter being stimulated with PHA was also lower than thosein normal controls (3.47±1.55 vs4.52±1.49, 34.03±2.94 vs37.95±3.00, P＜0.01). In all the patients with hepatitis B, thelevels of T lymphocyte subsets and mIL-2R in PBMC withHBV-DNA (+) were lower than those with HBV-DNA (-),which were significantly different (39.57±7.11 vs44.36±5.43,34.36±7.16 vs 40.75±5.87, 37.82±6.54 vs 41.72±6.21,0.88±0.33 vs0.99±0.27, 2.82±1.62 vs3.85±1.47, 31.56±3.00vs35.84±2.83, P＜0.01). In addition, the levels of CD3+, CD4+,CD8+ cells, the ratio of CD4+ cells/CD8+ cells and mIL-2R amongdifferent courses of hepatitis B were all significantly different(F=3 723.18, P＜0.01. F=130.43, P＜0.01. F=54.01, P＜0.01.F=2.99, P＜0.05. F=7.16, P＜0.01).CONCLUSION: Both cellular and humoral immune functionsare obviously in disorder in patients with hepatitis B, whichmight be closely associated with the chronicity in patients.
