Study Identifies Altered T Cell Profiles and IL-23/Th17 Pathway Dysregulation in Endometriosis
A new preprint study found significant immune dysregulation in endometriosis patients, particularly involving pathogenic Th17 cells and elevated inflammatory cytokines across blood, peritoneal fluid, and tissue samples. Researchers used cytokine profiling and bulk RNA sequencing to characterize T helper cell subsets across disease stages, identifying over 2,200 differentially expressed genes in Th17 cells alone. The findings suggest that therapies already approved for other inflammatory diseases — specifically those targeting IL-23 and IL-17 — could potentially be repurposed to treat endometriosis.
Researchers profiled immune mediators and performed RNA sequencing on T helper cell subsets from endometriosis patients and healthy controls, revealing widespread immune remodeling associated with the disease. Elevated levels of IL-6 were found in patient plasma, while FLT-3L and G-CSF were elevated in eutopic tissue, and IL-1RA and IL-23 (p40) were elevated in peritoneal fluid, particularly in severe-stage disease. Flow cytometry showed that pathogenic Th17 cells were significantly elevated in peritoneal fluid compared to non-pathogenic Th17 and regulatory T cell subsets. Interestingly, circulating Th17 cells were higher in mild-stage (I-II) than severe-stage (III-IV) endometriosis, suggesting dynamic immune shifts across disease progression. RNA sequencing identified 2,220 differentially expressed genes in Th17 cells, the most extensive reprogramming observed among the T helper subsets studied. The authors propose that IL-23- and IL-17-targeted biologics, already in clinical use for conditions like psoriasis and inflammatory bowel disease, represent a promising therapeutic avenue for endometriosis and its associated comorbidities.
What's missing
As a preprint, this study has not yet undergone peer review. The study does not report sample sizes or patient demographics in the abstract, limiting assessment of statistical power and generalizability. It is also unclear whether the observed immune alterations are causally linked to endometriosis pathogenesis or are secondary effects. No clinical trial data on IL-23/IL-17 inhibitors in endometriosis patients are presented, so therapeutic efficacy remains speculative at this stage.
What different sources said
- bioRxivCenter
An investigation of the IL-23/Th17 axis and transcriptomic profiles of T helper subsets in endometriosis
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