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<p>Inflammation is regulated by immune cells, with CD4<sup>+</sup> T cells playing a key role in its progression and resolution. Modulating their response is crucial for controlling inflammation, and mesenchymal stem cells (MSCs) have emerged as a promising therapeutic target due to their immunomodulatory properties. We previously showed that umbilical cord derived MSCs (UC-MSCs) induce a memory response in TCR-activated CD4<sup>+</sup> T cells, and here, we investigated the underlying mechanisms through gene expression analysis at different time points. Our results demonstrated that TCR activation is required for UC-MSCs to induce this memory response. Pathway analysis revealed that UC-MSCs induced the expression of genes that negatively regulate immune signalling pathways. This was further supported by phosphoflow cytometry, which showed suppression of the NF-κB and ERK pathways. Additionally, UC-MSCs enhanced the expression of genes related to CD4<sup>+</sup> T cell adhesion and migration at 12 and 24&#xa0;h. Notably, TNIP1 emerged as a potential key regulator of UC-MSCs-mediated immune modulation. This study provides new insights into how UC-MSCs influence CD4<sup>+</sup> T cell responses and highlights molecular targets for further investigation into UC-MSCs-driven immune regulation.</p>

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Mesenchymal stem cells suppress NF-κB and ERK signalling while enhancing chemotaxis in CD4+ T cells

  • 期刊论文

  • 出版模式：

    开放获取

  • 发表日期：

    2025年8月30日

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  • Ezgi Sengun,
  • Janeri Fröberg,
  • Xuehui He,
  • Marc Eleveld,
  • Ruben L. Smeets,
  • Hans J. P. M. Koenen,
  • Katja Möller-Hackbarth,
  • Tim G. A. M. Wolfs,
  • Daan R. M. G. Ophelders,
  • Martijn A. Huynen,
  • Marien I. de Jonge,
  • Renate G. van der Molen

摘要

Inflammation is regulated by immune cells, with CD4+ T cells playing a key role in its progression and resolution. Modulating their response is crucial for controlling inflammation, and mesenchymal stem cells (MSCs) have emerged as a promising therapeutic target due to their immunomodulatory properties. We previously showed that umbilical cord derived MSCs (UC-MSCs) induce a memory response in TCR-activated CD4+ T cells, and here, we investigated the underlying mechanisms through gene expression analysis at different time points. Our results demonstrated that TCR activation is required for UC-MSCs to induce this memory response. Pathway analysis revealed that UC-MSCs induced the expression of genes that negatively regulate immune signalling pathways. This was further supported by phosphoflow cytometry, which showed suppression of the NF-κB and ERK pathways. Additionally, UC-MSCs enhanced the expression of genes related to CD4+ T cell adhesion and migration at 12 and 24 h. Notably, TNIP1 emerged as a potential key regulator of UC-MSCs-mediated immune modulation. This study provides new insights into how UC-MSCs influence CD4+ T cell responses and highlights molecular targets for further investigation into UC-MSCs-driven immune regulation.