Nearly 10% of reproductive age women are affected by endometriosis globally, a condition in which the uterine tissue grows ectopically, resulting in pelvic pain and infertility. The peritoneal fluid (PF) surrounding ectopic endometrial tissue contains T helper 17 (Th17) cells. The number of Th17 cells in PF increases with disease severity; however, their function in endometriosis is unknown.
Recently, Jiang et al. used flow cytometry to detect and sort subpopulations of Th17 cells from the PF of patients with moderate to severe endometriosis. The researchers characterized several subsets of Th17 cells that could ultimately be defined by the presence or absence of four chemokine receptors, CCR4, CCR6, IL-17RE, and CD27. The presence of IL-17RE in particular correlated with an increase in Th17 cells in G1 and S-G2/M phase, suggesting increased cell proliferation. RNA-seq was used to further characterize this Th17 cellular subset.
The authors found an increase in oxidative phosphorylation and electron transport chain-related gene expression, which was validated with the Azure Cielo 3 and SYBR Green, thus identifying a pathological signature of a subset of Th17 cells associated with the disease. Additional experiments demonstrated an increase in adenosine triphosphate (ATP) production and reactive oxygen species (ROS), consistent with a role in mitochondrial respiration.
This work highlights the power of using gene expression analysis to characterize novel cellular subtypes relevant to disease. Next steps include determining whether the increase in ATP and ROS levels is a cause or effect of severe endometriosis. Interestingly, in mouse models of autoimmune kidney disease, decreased IL-17RE expression reduced the overall amount of Th17 cells, thus indicating a possible therapeutic target.
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