Victoria University of Wellington, Wellington, New Zealand; Wellington Cardiovascular Research Group, Wellington, New Zealand.
Victoria University of Wellington, Wellington, New Zealand; Wellington Cardiovascular Research Group, Wellington, New Zealand; Malaghan Institute of Medical Research, Wellington, New Zealand.
Atherosclerosis. 2015 Mar;239(1):283-6. doi: 10.1016/j.atherosclerosis.2015.01.006. Epub 2015 Jan 14.
While platelets have well characterized effects on monocytes, the effect of platelet activation on CD4+ T-cell differentiation and cytokine production is not clear. To examine the effects of platelet T-cell interactions on T-cell phenotype, and whether these interactions were altered by prasugrel, we conducted a randomized, double-blind, placebo-controlled crossover study in healthy subjects. At baseline the addition of platelets to CD4+ T-cells resulted in an increase in the release of pro-inflammatory cytokine IFN-γ (192% increase in IFN-γ levels, p = 0.01) and pro-inflammatory CD4+ phenotypes, (38% and 58% increase in Th1 and Th17 phenotypic markers respectively, p = 0.01) but no change in Tregs. Prasugrel abolished the effects of platelets on CD4+ T-cells with similar levels of pro-inflammatory cytokines and cell numbers to T-cells stimulated. Antiplatelet therapy may provide therapeutic benefit both from direct platelet inhibition and also through indirect effects on immune response development.
虽然血小板对单核细胞的作用已经得到了很好的描述，但血小板激活对 CD4+T 细胞分化和细胞因子产生的影响尚不清楚。为了研究血小板与 T 细胞相互作用对 T 细胞表型的影响，以及这些相互作用是否被普拉格雷改变，我们在健康受试者中进行了一项随机、双盲、安慰剂对照的交叉研究。在基线时，将血小板添加到 CD4+T 细胞中会导致促炎细胞因子 IFN-γ 的释放增加（IFN-γ 水平增加 192%，p=0.01）和促炎 CD4+表型增加（Th1 和 Th17 表型标志物分别增加 38%和 58%，p=0.01），但 Treg 没有变化。普拉格雷消除了血小板对 CD4+T 细胞的作用，其促炎细胞因子和细胞数量与刺激的 T 细胞相似。抗血小板治疗可能不仅通过直接抑制血小板，而且还通过对免疫反应发展的间接影响提供治疗益处。
