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<p>Autoantigen−specific CD4<sup>+</sup> T cells are central to the development of autoimmune diseases, while the expansion of regulatory T (Treg) cells expressing Forkhead box protein 3 (Foxp3) is essential for mitigating these conditions. In this study, we identified CD4<sup>+</sup>Notch2<sup>+</sup>Foxp3<sup>lo</sup> T cells in the spinal cords of mice with experimental autoimmune encephalomyelitis (EAE), dextran sodium sulfate−induced colitis model mice, and patients with ulcerative colitis as immune regulatory cells. These cells exhibited a nonproliferative, dysfunctional phenotype and demonstrated immune regulatory functions, including suppressive activity against activated CD4<sup>+</sup> T cells and marked Treg cell expansion activity. Our data revealed that Notch2 deletion in Foxp3−expressing cells diminishes the ability of this population to reverse the clinical symptoms of EAE. Collectively, these findings suggest that Notch2 expression in dysfunctional CD4<sup>+</sup> T cells plays a crucial role in immune regulation.</p>

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Notch2−expressing CD4+ T cells attain immunoregulatory functions during autoimmune inflammation

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年7月23日

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  • So-Eun Bae,
  • Sang-Heon Park,
  • Chae Youn Kim,
  • Cho-Rong Lee,
  • Chanyeon Lee,
  • Rosah May Payumo,
  • So Yeon Kim,
  • Kyu-Young Sim,
  • Ho Jin Kim,
  • Hyungseok Seo,
  • Seong-Joon Koh,
  • Seunghee Hong,
  • Sung-Gyoo Park

摘要

Autoantigen−specific CD4+ T cells are central to the development of autoimmune diseases, while the expansion of regulatory T (Treg) cells expressing Forkhead box protein 3 (Foxp3) is essential for mitigating these conditions. In this study, we identified CD4+Notch2+Foxp3lo T cells in the spinal cords of mice with experimental autoimmune encephalomyelitis (EAE), dextran sodium sulfate−induced colitis model mice, and patients with ulcerative colitis as immune regulatory cells. These cells exhibited a nonproliferative, dysfunctional phenotype and demonstrated immune regulatory functions, including suppressive activity against activated CD4+ T cells and marked Treg cell expansion activity. Our data revealed that Notch2 deletion in Foxp3−expressing cells diminishes the ability of this population to reverse the clinical symptoms of EAE. Collectively, these findings suggest that Notch2 expression in dysfunctional CD4+ T cells plays a crucial role in immune regulation.