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Publications

Journal Article Ppublish

PubMed: 40205945 DOI: 10.3724/abbs.2024178

Decreased CCL5 expression in endometrial stromal cells induces deficient CCR5 +CD4 + T cells in endometriosis.

Acta Biochim Biophys Sin (Shanghai) 57(5):690-700

Authors: Yue Li, Yunyun Li, Yewei Lu, Yikong Lin, Xiaolin Wang, Yizhun Zhu, Qiongjing Zeng, Meirong Du

Affiliations

  • State Key Laboratory of Quality Research in Chinese Medicine and School of Pharmacy, Macau University of Science and Technology, Macau SAR, China. Department of Obstetrics and Gynecology, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai 200092, China. Laboratory of Reproduction Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Obstetrics and Gynecology Hospital and Institute, Fudan University Shanghai Medical College, Shanghai 200433, China.
  • Department of Reproductive Medical Center, West China Second University Hospital, Sichuan University, Chengdu 610065, China. Key Laboratory of Birth Defects and Related Diseases of Women and Children (Sichuan University), Ministry of Education, Sichuan University, Chengdu 610065, China.
  • State Key Laboratory of Quality Research in Chinese Medicine and School of Pharmacy, Macau University of Science and Technology, Macau SAR, China.
  • Laboratory of Reproduction Immunology, Shanghai Key Laboratory of Female Reproductive Endocrine Related Diseases, Obstetrics and Gynecology Hospital and Institute, Fudan University Shanghai Medical College, Shanghai 200433, China.
  • Department of Obstetrics and Gynecology, Shanghai Fourth People's Hospital, School of Medicine, Tongji University, Shanghai 200092, China.

Abstract

Endometriosis (EMS) is a benign gynecological disease characterized by the growth of endometrial tissue outside the uterine cavity. Evidence shows that the survival of patients with ectopic endometrial implants is associated with a dysregulated immune microenvironment. CD4 + T cells can regulate EMS through diverse cytokines, the inflammatory response, and angiogenesis. CCR5 +CD4 + T cells exhibit increased cellular immunogenicity and play a role in infectious diseases, host defense, and cancer progression. However, the specific mechanisms of CCR5 +CD4 + T cells in EMS remain unknown. In the present study, flow cytometry and RNA-seq are utilized to assess the proportions and features of CCR5 +CD4 + T cells in EMS patients, RT-PCR and ELISA are used to assess the production of CCL5 by ectopic endometrial stromal cells (ecESCs). Two EMS models are established through C57B6 wild-type and CCL5 ‒/‒ mice and utilized to explore the in vivo effects of CCR5 +CD4 + T cells on ectopic lesions. Compared with CCR5 ‒CD4 + T cells, CCR5 +CD4 + T cells display a more activated and cytotoxic phenotype. Diminished CCR5 +CD4 + T cells and their impaired ability to produce IFN-γ are observed in the ectopic lesions of EMS patients and in murine EMS models. Impaired production of CCL5 has been detected in human ecESCs. Moreover, endometria stripped from CCL5 ‒/‒ mice are more likely to generate ectopic lesions in the peritoneum of recipient mice. These findings demonstrate that the attenuated recruitment of CCR5 +CD4 + T cells in ectopic lesions caused by decreased production of CCL5 in ecESCs may facilitate the progression of EMS.

MeSH

Endometriosis, Cells, Biophysics, Endometrium, Stromal Cells, Wounds And Injuries