Résumé
Acute coronary syndrome (ACS) is a cardiac acute ischemic syndrome caused by the rupture or erosion of unstable atherosclerotic plaques within the coronary artery, leading to thrombus formation. Antiplatelet therapy is a key strategy in treating ACS, and although some success has been achieved, there are still limitations, such as thrombus recurrence and bleeding side effects, which limit the long-term use of drugs. Future antiplatelet therapies may achieve more effective or safer treatment methods by targeting novel targets involved in platelet function. This article focuses on potential target inhibitors, including GPVI, protease -activated receptor (PAR) - 4, GPIb, 5-hy-droxytryptamine receptor subtype 2A (5-HT2A), protein disulfide isomerase, P-selectin, and phosphatidylinositol 3-kinase β inhibitors.
Résumé
Objective To elucidate the influences of epitope competition on the frequency and average intensity of specific T cell response.Methods C57BL/6 mice were immunized with either single epitope DNA vaccines (pSV-gag92 or pSV-env203) or fusion gene DNA vaccine (pSV-gag/env).Gag92and Env203 epitope-specific CD8 T cell responses were analyzed by intracellular cytokine staining assay.Results Gag92-specific IFN-γ+CD8 T cells that were induced by pSV-gag92 accounted for 0.415 00％ ±0.045 88％ of the total CD8 T cells,which was much more than that induced by pSV-gag/env of 0.058 67％ + 0.019 64％.Moreover,the mean fluorescence intensity of Gag92-specific TNF-α-IFN-γ+CD8 T cells (296.70+14.08) elicited by pSV-gag/env was significantly lower than that of Env203-specific TNF-α-IFN-γ+CD8 T cells (818.00+49.34).Conclusion Epitope competition could significantly decrease both the frequency and the average intensity of specific T cell response to subdominant epitopes.