Department: Molecular Pathology & Immunology
Faculty Mentor: Kevin Osteen, Ph.D.
Dissertation Description: Modeling the Immunological Origin(s) of the “Endometriosis/Adenomyosis Phenotype
Endometriosis, the ectopic growth of endometrial tissue, affects approximately 10-15% of reproductive age women and is a leading cause of infertility. It is an estrogen dependent disease; however, up to 70% of affected women exhibit progesterone (P4) resistance. The anti-inflammatory actions of P4 are critical to normal endometrial function and establishment and maintenance of pregnancy. Thus, a loss of P4 action likely promotes progression of endometriosis following repeat cycles of retrograde menstruation. Our group is exploring whether exposure to the environmental endocrine disruptor dioxin provides a mechanistic link between altered systemic immune function, the development of endometrial P4 insensitivity, and adenomyosis, ectopic endometrial tissues within the uterine muscle. The goal of my project is to determine the specific contribution of altered immune cell function to reduced P4 sensitivity within the uterus and the potential utility of using immune cells as a diagnostic/therapeutic target.