Our results suggest that reduced immune cell cytotoxicity is a bigger driver of disease onset than immune cell detection. We also observe that once the system shifts into a diseased state, restoring immune function may require a significantly greater effort to clear the disease.

Results show the presence of increased levels of retrograde menstruation alone is not a predictor of disease level. This aligns with previous studies showing the prevalence of retrograde menstruation is higher than the prevalence of endometriosis.

Our compartmental model focuses on interactions between macrophages, natural killer cells, and ectopic endometrial cells during the initial stages of lesion formation, and we explore the response to changes in the levels of retrograde menstruation, immune cell detection, and immune cell clearance.

In this study, we explore how the immune system contributes to the early stages of endometriosis lesion onset, focusing on the interactions between innate immune cells and endometrial cells in the peritoneal fluid.