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Elevated interleukin-33, CD1c+ dendritic cells, and interleukin-17A in peritoneal fluid of patients with endometriosis: a case-control study
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DOI：10.1007/s11033-026-12457-8.png)
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Abstract
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Endometriosis (EMS) is a chronic inflammatory disorder involving ectopic endometrial tissue growth. This study investigated IL-33, CD1c+ dendritic cells (DCs) and their co-stimulatory molecules (CD40, CD80, CD86), and IL-17 A in the peritoneal fluid (PF) of EMS patients, and explored their interrelationships. PF samples were obtained from 42 women with EMS as experimental subjects and 31 women without EMS as controls. Enzyme-linked immunosorbent assay (ELISA) showed that PF IL-33 (P < 0.001) and IL-17 A (P < 0.01) levels were significantly elevated in EMS patients vs. controls. Moreover, IL-33 levels were significantly higher in stages III–IV than I–II (P < 0.01). Flow cytometry (FCM) revealed no significant difference in the proportion of CD1c + DCs within EMS patient PF compared to controls (P > 0.05). However, the proportions of CD1c+CD40+ (P < 0.001), CD1c+CD80+ (P < 0.05), and CD1c+CD86+ (P < 0.01) DCs were significantly elevated in EMS, with CD1c+CD40 + higher in stages III–IV vs. I–II (P < 0.05). For in vitro experiments, control PF mononuclear cells (PFMCs) were incubated with recombinant IL-33 (100 ng/mL) for 24 h. IL-33 treatment increased IL-17 A production and CD1c+CD40 + and CD1c+CD80 + DC frequences in control PFMCs compared to unstimulated PFMCs (all P < 0.05). Elevated IL-33 and IL-17 A levels, along with enhanced CD1c + DC maturation and activation in PF, may contribute to EMS pathogenesis and progression. IL-33 may promote disease development by inducing CD1c + DC maturation/activation, thus increasing IL-17 A production.
Keywords:
Endometriosis
Peritoneal fluid
IL-33
IL-17A
CD1c+
Dendritic cells
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