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Background <p>Pro-EGCG has shown therapeutic promise for endometriosis, yet its immunoregulatory mechanisms remain unclear. Myeloid-derived suppressor cells (MDSCs) are key drivers of disease progression. This study investigates whether Pro-EGCG alleviates endometriosis by modulating MDSC-mediated immune and stromal dysregulation.</p> Methods <p>The therapeutic effects of Pro-EGCG were evaluated in an experimental endometriosis mouse model by assessing lesion burden, histology, and MDSC dynamics. The functional necessity of monocytic MDSCs (M-MDSCs) was validated via adoptive transfer. Clinical relevance was assessed in peripheral blood and lesions from women with or without endometriosis via flow cytometry and multiplex immunofluorescence staining. Furthermore, the direct effects of Pro-EGCG on human PBMC-derived M-MDSCs were examined <i>in vitro</i>, including their immunosuppressive function and their ability to promote fibrosis in a co-culture system with human endometriotic stromal cells.</p> Results <p>In the mouse model, Pro-EGCG treatment significantly reduced lesion weight, volume, and fibrosis, accompanied by consistent M-MDSC reduction systemically and locally. Lesion-infiltrating M-MDSCs, rather than polymorphonuclear MDSCs (PMN-MDSCs), positively correlated with disease severity. Adoptive transfer of M-MDSCs reversed Pro-EGCG’s therapeutic effects. In clinical samples, data confirmed a significant expansion of M-MDSCs in patients with endometriosis compared to controls. <i>In vitro</i>, Pro-EGCG compromised human M-MDSC survival and impaired their suppressive capacity by inhibiting ROS, Arg-1, and NO production. Furthermore, M-MDSC-induced stromal cell proliferation and fibrotic gene expression were abolished by Pro-EGCG preconditioning.</p> Conclusion <p>Pro-EGCG hinders endometriosis progression by inhibiting M-MDSC accumulation, immunosuppressive functions, and pro-endometriotic activities. These findings position Pro-EGCG as a potential immunotherapy for endometriosis and other M-MDSC-driven inflammatory disorders.</p>

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Pro-EGCG suppresses endometriosis progression via regulating monocytic myeloid-derived suppressor cells

  • 期刊论文

  • 出版模式：

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  • 发表日期：

    2026年7月1日

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  • Qianhan Xu,
  • Lu Chen,
  • Jun Chen,
  • Haoyue Hu,
  • Zhihua Luo,
  • Zhentao Gong,
  • Yee Lee Ng,
  • Jinchuan Liu,
  • Sze Wan Hung,
  • Yi Song,
  • Nga Ping Ip,
  • See Yung Chau,
  • Yonggang Duan,
  • Chi Chiu Wang,
  • Ting Guo,
  • Kam Tong Leung,
  • Jingying Zhou,
  • Pui Wah Chung,
  • Tao Zhang

摘要

Background

Pro-EGCG has shown therapeutic promise for endometriosis, yet its immunoregulatory mechanisms remain unclear. Myeloid-derived suppressor cells (MDSCs) are key drivers of disease progression. This study investigates whether Pro-EGCG alleviates endometriosis by modulating MDSC-mediated immune and stromal dysregulation.

Methods

The therapeutic effects of Pro-EGCG were evaluated in an experimental endometriosis mouse model by assessing lesion burden, histology, and MDSC dynamics. The functional necessity of monocytic MDSCs (M-MDSCs) was validated via adoptive transfer. Clinical relevance was assessed in peripheral blood and lesions from women with or without endometriosis via flow cytometry and multiplex immunofluorescence staining. Furthermore, the direct effects of Pro-EGCG on human PBMC-derived M-MDSCs were examined in vitro, including their immunosuppressive function and their ability to promote fibrosis in a co-culture system with human endometriotic stromal cells.

Results

In the mouse model, Pro-EGCG treatment significantly reduced lesion weight, volume, and fibrosis, accompanied by consistent M-MDSC reduction systemically and locally. Lesion-infiltrating M-MDSCs, rather than polymorphonuclear MDSCs (PMN-MDSCs), positively correlated with disease severity. Adoptive transfer of M-MDSCs reversed Pro-EGCG’s therapeutic effects. In clinical samples, data confirmed a significant expansion of M-MDSCs in patients with endometriosis compared to controls. In vitro, Pro-EGCG compromised human M-MDSC survival and impaired their suppressive capacity by inhibiting ROS, Arg-1, and NO production. Furthermore, M-MDSC-induced stromal cell proliferation and fibrotic gene expression were abolished by Pro-EGCG preconditioning.

Conclusion

Pro-EGCG hinders endometriosis progression by inhibiting M-MDSC accumulation, immunosuppressive functions, and pro-endometriotic activities. These findings position Pro-EGCG as a potential immunotherapy for endometriosis and other M-MDSC-driven inflammatory disorders.