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<p>Primary Immune Thrombocytopenia (ITP) is characterized by reduced immunosuppressive function of regulatory T cells (Tregs), contributing to immune imbalance and decreased platelet counts. However, the mechanisms behind this reduced efficacy of Tregs remain unclear. Our study used a variety of methods, including Treg function assays, cytokine analysis, and single-cell sequencing, to explore these mechanisms. We found that exosomes from ITP patients inhibited TBX21 expression in Tregs, and impaired their ability to suppress Th1 cells. At the single-cell level, Tregs with high TBX21 expression were identified, and the activity of the TBX21 regulon was found to be enhanced in early-stage Treg subpopulations. We also discovered that ARID3A interacted with SPI1 and TBX21 gene regions, indicating a regulatory relationship between ARID3A, SPI1, and TBX21. Additionally, exosomes in ITP patients' plasma contained elevated levels of miR-363-3p, which negatively correlated with platelet count. These exosomes transferred miR-363-3p to Tregs, downregulating ARID3A, SPI1, and TBX21 expression, thereby weakening Tregs' ability to suppress conventional CD4 + T cells. In conclusion, exosomes from ITP patients reduced Treg function through the ARID3A/SPI1/TBX21 axis by miR-363-3p, diminishing their ability to regulate Th1 cells and contributing to the immune dysfunction observed in ITP.</p>

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Plasma Exosomes Derived from Patients with Primary Immune Thrombocytopenia Attenuate TBX21+ Regulatory T Cell-Mediated Immune Suppression via MiR-363-3p

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2025年3月4日

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  • Yuanlan Huang,
  • Peng Liu,
  • Ying Xu,
  • Cheng Qian,
  • Tianqin Wu,
  • Tengda Li

摘要

Primary Immune Thrombocytopenia (ITP) is characterized by reduced immunosuppressive function of regulatory T cells (Tregs), contributing to immune imbalance and decreased platelet counts. However, the mechanisms behind this reduced efficacy of Tregs remain unclear. Our study used a variety of methods, including Treg function assays, cytokine analysis, and single-cell sequencing, to explore these mechanisms. We found that exosomes from ITP patients inhibited TBX21 expression in Tregs, and impaired their ability to suppress Th1 cells. At the single-cell level, Tregs with high TBX21 expression were identified, and the activity of the TBX21 regulon was found to be enhanced in early-stage Treg subpopulations. We also discovered that ARID3A interacted with SPI1 and TBX21 gene regions, indicating a regulatory relationship between ARID3A, SPI1, and TBX21. Additionally, exosomes in ITP patients' plasma contained elevated levels of miR-363-3p, which negatively correlated with platelet count. These exosomes transferred miR-363-3p to Tregs, downregulating ARID3A, SPI1, and TBX21 expression, thereby weakening Tregs' ability to suppress conventional CD4 + T cells. In conclusion, exosomes from ITP patients reduced Treg function through the ARID3A/SPI1/TBX21 axis by miR-363-3p, diminishing their ability to regulate Th1 cells and contributing to the immune dysfunction observed in ITP.