Bile acid receptor TGR5 has been proved to play protective roles in the process of myocardial infarction (MI). Recently, we found spleen weight of Tgr5^+/+ mice was increased at 7-day post-MI but not in Tgr5^−/− mice. Since the spleen is one of the main resources of immune and inflammatory cells post-MI, we conducted flow cytometry analysis of multiple immune cells in the heart post-MI. It showed the recruitment of CD4⁺ T cells and CD8⁺ T cells was continuously more in the heart of Tgr5^−/− mice post-MI until 7 days after MI. Furthermore, CD4-specific TGR5 depletion mice exhibited aggravated ischemic injury. The mRNA expressions of the markers of Th1 and Treg were upregulated in the heart of Tgr5^−/− mice at 7-day post-MI. These results suggested TGR5 modulates CD4⁺ T cell functions and subsets distribution in the heart, and plays protective roles in myocardial infarction.

Graphical abstract

中文翻译：

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TGR5 在心肌梗死 CD4+ T 细胞功能调节中的作用和机制

胆汁酸受体 TGR5 已被证明在心肌梗死 (MI) 过程中起保护作用。最近，我们发现Tgr5 ^{+ / +}小鼠的脾脏重量在 MI 后 7 天增加，但在Tgr5 ^-/-小鼠中没有。由于脾脏是 MI 后免疫和炎症细胞的主要来源之一，我们对 MI 后心脏中的多个免疫细胞进行了流式细胞术分析。它表明 CD4 ⁺ T 细胞和 CD8 ^{+ T 细胞在}Tgr5的心脏中持续增加^-/-MI 后的小鼠直至 MI 后 7 天。此外，CD4 特异性 TGR5 耗竭小鼠表现出加重的缺血性损伤。在心肌梗死后 7 天， Tgr5 ^-/-小鼠心脏中 Th1 和 Treg 标志物的 mRNA 表达上调。这些结果表明TGR5调节心脏中CD4 ⁺ T细胞功能和亚群分布，并在心肌梗死中起保护作用。

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