Scholarlink

<p>Recent studies found that treatment with an anti-T-cell immunoglobulin mucin-1 (TIM1) monoclonal antibody (RMT1-10) regulated immune responses by inducing regulatory B cells (Bregs). However, the role of these cells in myocardial ischemia-reperfusion injury (IRI) is unknown. This study aimed to investigate the protective effect of RMT1-10 on myocardial IRI and its potential mechanism. We established a myocardial IRI model, and Triphenyl tetrazolium chloride staining, Terminal deoxynucleotidyl transferase nick-end-labeling, hematoxylin and eosin, and transmission electron microscopy were performed to examine the myocardial infarction size, myocardial cell apoptosis, and cardiomyocyte morphology and structure. The data showed that RMT1-10 could alleviate myocardial IRI, increase the number of TIM1<sup>+</sup>Bregs and interleukin 10 (IL-10) secretion, and regulate the expression of inflammatory factors after myocardial IRI. However, treatment with RMT1-10 and Anti-CD20 abrogated the protective effect of RMT-10. In addition, RMT1-10 treatment inhibited T cells but significantly activated Tregs after IRI, while RMT1-10 combined with Anti-CD20 abolished this effect on Tregs. Furthermore, sequencing analysis showed marked expression changes among genes related to several classical signaling pathways in response to RMT1-10. Taken together, these findings indicated that RMT1-10 could increase the number of TIM1<sup>+</sup> Bregs and regulate IL-10-mediated inflammatory reactions, activate Tregs to inhibit inflammation, and might regulate the above-mentioned signaling pathways to protect against myocardial IRI.</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

The effect of TIM1+ Breg cells in myocardial ischemia-reperfusion injury

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年10月7日

查看全文
  • Cong Zeng,
  • Jianchuan Qi,
  • Feifei Wu,
  • Weijun Yang,
  • Minjian Kong,
  • Haifeng Cheng,
  • Aiqiang Dong,
  • Jie Han,
  • Wei Chen,
  • Dajin Chen,
  • Qunjun Duan

摘要

Recent studies found that treatment with an anti-T-cell immunoglobulin mucin-1 (TIM1) monoclonal antibody (RMT1-10) regulated immune responses by inducing regulatory B cells (Bregs). However, the role of these cells in myocardial ischemia-reperfusion injury (IRI) is unknown. This study aimed to investigate the protective effect of RMT1-10 on myocardial IRI and its potential mechanism. We established a myocardial IRI model, and Triphenyl tetrazolium chloride staining, Terminal deoxynucleotidyl transferase nick-end-labeling, hematoxylin and eosin, and transmission electron microscopy were performed to examine the myocardial infarction size, myocardial cell apoptosis, and cardiomyocyte morphology and structure. The data showed that RMT1-10 could alleviate myocardial IRI, increase the number of TIM1+Bregs and interleukin 10 (IL-10) secretion, and regulate the expression of inflammatory factors after myocardial IRI. However, treatment with RMT1-10 and Anti-CD20 abrogated the protective effect of RMT-10. In addition, RMT1-10 treatment inhibited T cells but significantly activated Tregs after IRI, while RMT1-10 combined with Anti-CD20 abolished this effect on Tregs. Furthermore, sequencing analysis showed marked expression changes among genes related to several classical signaling pathways in response to RMT1-10. Taken together, these findings indicated that RMT1-10 could increase the number of TIM1+ Bregs and regulate IL-10-mediated inflammatory reactions, activate Tregs to inhibit inflammation, and might regulate the above-mentioned signaling pathways to protect against myocardial IRI.