• CCR5+CD4+ T cells exhibit a more activated and cytotoxic phenotype compared to CCR5‒CD4+ T cells, with diminished numbers and impaired IFN-γ production in endometriosis lesions.
• Ectopic endometrial stromal cells (ecESCs) show impaired production of CCL5, leading to reduced recruitment of CCR5+CD4+ T cells.
• CCL5 knockout mice develop larger ectopic lesions, confirming the protective role of CCL5-CCR5 axis in endometriosis progression.
• The study suggests that enhancing CCL5 expression or CCR5+CD4+ T cell recruitment could be a potential therapeutic strategy for endometriosis.