Scholarlink

<p>Treatment with PD-1 inhibitors may cause immune-related adverse events (irAE), of which PD-1 inhibitor-associated myocarditis is a rare and highly lethal irAE. However, the mechanism of PD-1 inhibitors-induced myocarditis in individuals with tumor is still unclear. Regulatory T cells (Treg) can directly inhibit T cell proliferation and activation, and also produce inhibitory cytokines with potent immunosuppressive properties. Deletion or aberrant function of Treg usually leads to autoimmune diseases. But reports on the role of Treg in PD-1 inhibitor-associated myocarditis are still very limited, and its role in the pathogenesis of myocarditis needs to be further explored. In addition, alterations in the composition of the gut microbiota and its metabolites have been shown to be involved in the development of several cardiovascular and autoimmune diseases. Therefore, we designed this experiment initially to investigate the role of gut microbiota in PD-1 inhibitor-associated myocarditis. Our studies showed that PD-1 inhibitors induced myocarditis and significant reduction of intracardiac Tregs in melanoma mice. It is highly likely that alterations in the composition of the gut microbiota due to PD-1 inhibitors played a key role in this process.</p>

错误：搜索内容不能为空，请输入英文关键词
错误：关键词超出字数限制，请精简
高级检索

Abnormal gut microbiota may cause PD-1 inhibitor-related cardiotoxicity via suppressing regulatory T cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年7月1日

查看全文
  • Huili Cao,
  • Huwei Dai,
  • Songshan Li,
  • Zeeshan Afzal,
  • Xinyan Wang,
  • Zeyu Wen,
  • Kaiyong Xiao,
  • Yajing Zhao,
  • Jin Li,
  • Bin Yang

摘要

Treatment with PD-1 inhibitors may cause immune-related adverse events (irAE), of which PD-1 inhibitor-associated myocarditis is a rare and highly lethal irAE. However, the mechanism of PD-1 inhibitors-induced myocarditis in individuals with tumor is still unclear. Regulatory T cells (Treg) can directly inhibit T cell proliferation and activation, and also produce inhibitory cytokines with potent immunosuppressive properties. Deletion or aberrant function of Treg usually leads to autoimmune diseases. But reports on the role of Treg in PD-1 inhibitor-associated myocarditis are still very limited, and its role in the pathogenesis of myocarditis needs to be further explored. In addition, alterations in the composition of the gut microbiota and its metabolites have been shown to be involved in the development of several cardiovascular and autoimmune diseases. Therefore, we designed this experiment initially to investigate the role of gut microbiota in PD-1 inhibitor-associated myocarditis. Our studies showed that PD-1 inhibitors induced myocarditis and significant reduction of intracardiac Tregs in melanoma mice. It is highly likely that alterations in the composition of the gut microbiota due to PD-1 inhibitors played a key role in this process.