Graduation Year

2026

Date of Submission

12-2025

Document Type

Campus Only Senior Thesis

Degree Name

Bachelor of Arts

Department

Biology

Reader 1

Mihoko Kato

Reader 2

Diana Williams

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© 2025 Elizabeth L Gutierrez

Abstract

Endometriosis is a chronic gynecological disease where endometrial tissue spreads outside of the uterus and creates painful lesions that may require surgery to resolve. Patients consistently exhibit immune system dysregulation, resulting in a pro-inflammatory environment compared to healthy patients. Estrogen is known to worsen endometriosis lesion development and affect immune cell recruitment pathways, but the mechanism by which this happens is still unclear. Several cells have been investigated for displaying altered immune profiles during endometriosis, including endometrial mesenchymal stem cells (eMSCs). eMSCs support the endometrium during tissue regeneration and demonstrate some immune regulation properties. This proposal aims to investigate the changes in gene expression of cytokine modulators and cytokine proliferation patterns exhibited by eMSCs in endometriosis patients, and how those changes are altered in the presence of estrogen. It is expected that overall immunoreactive genes will be upregulated while immunosuppressive genes will be downregulated. Cytokine proliferation is expected to follow a similar pattern. In the presence of estrogen, cells derived from non-endometriosis patients are expected to exhibit alterations of gene expression and cytokine proliferation that mimic results from endometriosis cells. This would indicate that increased estrogen is a driver of immunoreactivity. This research could clarify how estrogen alters immune cell recruitment and supports endometriosis lesion development. Identifying such a mechanism would enable the development of precise therapeutics that go beyond ameliorating symptoms and instead target the drivers of endometriosis lesion development.

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