Dendritic Cell Mediated Heat-Shock Protein 60 Specific T Cytotoricity in Acute Coronary Syndrome
Wei Wu
Abstract
Wei Wu
Abstract
Objective: To investigate whether dendritic cells ( DC ) derived from patients with acute coronary syndrome (ACS) can induce heat-shock protein 60 (HSP60) specific T cell immune response to endothelial cells. Methods : DCs generated from peripheral blood mononuclear cells of 20 patients with ACS, 15 patients with stable angina and 10 healthy subjects were investigated. CD86 expression on HSP60-pulsed and no-pulsed DCs,and percentage of CD45RO+T cells were detected by flow cytometry. MTT was used to assay the ability of DCs from each group to stimulate autologous T cell proliferation and cytotoxic T lymphocytes (CTL) mediated lysis of HSP60 loaded endothelial cells. ELISA was used to assay inter-ferin-γ release by T cells. Results: Compared with DCs from stable angina and healthy subjects, CD86 was much more expressed in DCs from ACS and from DCS pulsed with HSP60. Capacity of DCs from ACS and from DCs pulsed with HSP60 to stumulate autologous T cell proliferation was increased; DCs from ACS and pulsed with HSP60 could induce HSP60 specific CTLs which could efficiently kill endothelial cells loading HSP60. Percentage of HSP60 specific CD45RO+ memory T cells was higher in ACS. Conclusion: There exists DC- mediated HSP60 specific T cell cytotoxity in acute coronary syndrome.
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Objective: To investigate whether dendritic cells ( DC ) derived from patients with acute coronary syndrome (ACS) can induce heat-shock protein 60 (HSP60) specific T cell immune response to endothelial cells. Methods : DCs generated from peripheral blood mononuclear cells of 20 patients with ACS, 15 patients with stable angina and 10 healthy subjects were investigated. CD86 expression on HSP60-pulsed and no-pulsed DCs,and percentage of CD45RO+T cells were detected by flow cytometry. MTT was used to assay the ability of DCs from each group to stimulate autologous T cell proliferation and cytotoxic T lymphocytes (CTL) mediated lysis of HSP60 loaded endothelial cells. ELISA was used to assay inter-ferin-γ release by T cells. Results: Compared with DCs from stable angina and healthy subjects, CD86 was much more expressed in DCs from ACS and from DCS pulsed with HSP60. Capacity of DCs from ACS and from DCs pulsed with HSP60 to stumulate autologous T cell proliferation was increased; DCs from ACS and pulsed with HSP60 could induce HSP60 specific CTLs which could efficiently kill endothelial cells loading HSP60. Percentage of HSP60 specific CD45RO+ memory T cells was higher in ACS. Conclusion: There exists DC- mediated HSP60 specific T cell cytotoxity in acute coronary syndrome.
Key concepts: CD86, Cytotoxic T cell, Medicine, HSP60, T cell, Flow cytometry, Immunology, Immune system