T cells play vital roles in the development and progression of acute coronary syndromes (ACS), including cytotoxicity mediated by CD8⁺ T cells and immunoregulatory activity mediated by CD4⁺ T cells. Interleukin (IL)‐9‐secreting CD4⁺ T cells (Th9 cells) were recently found to be involved in the onset of ACS. We investigated regulatory role of Th9 cells to CD8⁺ T cells in patients with stable angina pectoris, unstable angina pectoris, and acute myocardial infarction (AMI). Circulating Th9 cells percentage, plasma IL‐9 level, and PU.1 mRNA relative level was up‐regulated in AMI patients compared with controls. There was no significant difference of IL‐9‐secreting CD8⁺ T cells percentage among groups. CD8⁺ T cells from AMI patients revealed increased cytotoxicity than those from controls, which presented as enhanced cytotolytic activity to target cells, increased interferon‐γ and tumor necrosis factor‐α secretion, elevated perforin and granzyme B production, and reduced programmed death‐1 and cytotoxic T lymphocyte‐associated protein 4. IL‐9 stimulation did not affect proliferation, but promoted CD8⁺ T‐cell cytotoxicity from both controls and AMI patients. IL‐9‐secreting CD4⁺ T cells were enriched in CD4⁺CCR4⁻CCR6⁻CXCR3⁻ cells. The enhancement of CD8⁺ T‐cell cytotoxicity induced by CD4⁺CCR4⁻CCR6⁻CXCR3⁻ cells was dependent on IL‐9 secretion. The present results indicated that up‐regulation of IL‐9‐secreting CD4⁺ T cells may contribute to pathogenesis of AMI through enhancement of CD8⁺ T‐cell cytotoxicity.

中文翻译：

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白细胞介素9分泌的CD4 + T细胞调节急性冠脉综合征患者的CD8 + T细胞细胞毒性

T细胞在急性冠状动脉综合征（ACS）的发生和发展中起着至关重要的作用，包括CD8 ⁺ T细胞介导的细胞毒性和CD4 ⁺ T细胞介导的免疫调节活性。最近发现分泌白介素（IL）-9的CD4 ⁺ T细胞（Th9细胞）与ACS的发作有关。我们调查了稳定型心绞痛，不稳定型心绞痛和急性心肌梗死（AMI）患者中Th9细胞对CD8 ⁺ T细胞的调节作用。与对照组相比，AMI患者的循环Th9细胞百分比，血浆IL-9水平和PU.1 mRNA相对水平上调。各组之间IL-9分泌CD8 ⁺ T细胞的百分比没有显着差异。CD8AMI患者的⁺ T细胞显示出比对照组更高的细胞毒性，表现为对靶细胞的细胞溶解活性增强，干扰素-γ和肿瘤坏死因子-α分泌增加，穿孔素和颗粒酶B产生增加以及程序性死亡-1和细胞毒性T淋巴细胞相关蛋白4. IL-9刺激并未影响增殖，但从对照组和AMI患者中促进了CD8 ⁺ T细胞的细胞毒性。分泌IL-9的CD4 ⁺ T细胞富含CD4 ⁺ CCR4 ⁻ CCR6 ⁻ CXCR3 ⁻细胞。CD4 ⁺ CCR4诱导的CD8 ⁺ T细胞细胞毒性增强^-CCR6 ^- CXCR3 ^-细胞是依赖于IL-9的分泌。目前的结果表明，分泌IL-9的CD4 ⁺ T细胞上调可能通过增强CD8 ⁺ T细胞的细胞毒性来促进AMI的发病。