Complement Component 3 expressed by the endometrial ectopic tissue is involved in the endometriotic lesion formation through mast cell activation
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Complement component 3 produced by ectopic endometrial tissue drives endometriotic lesion formation by activating mast cells.
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Abstract
Abstract The pathophysiology of endometriosis (EM) is an excellent example of immune dysfunction, reminiscent of tumor microenvironment as well. Here, we report that an interplay between C3 and mast cells (MCs) is involved in the pathogenesis of ectopic EM. C3 is at the epicenter of the regulatory feed forward loop, amplifying the inflammatory microenvironment, in which the MCs are protagonists. Thus, C3 can be considered a marker of EM and its local synthesis can promote the engraftment of the endometriotic cysts. We generated a murine model of EM via injection of minced uterine tissue from a donor mouse, into the peritoneum of the recipient mice. The wild type mice showed greater amount of cyst formation in the peritoneum compared to C3 knock-out mice. This study offers an opportunity for novel therapeutic intervention in EM, a difficult to treat gynecological condition. Summary C3 produced by the endometriotic tissue is involved in the lesion development through mast cell activation
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Cited by (7)
- Evaluation of serum and peritoneal fluid mannose‐binding lectin associated serine protease‐3, adipsin, properdin, and complement factor‐H levels in endometriosis patients 2025
- Endometriosis as an autoimmune disease 2024
- Proteomics approach to discovering non-invasive diagnostic biomarkers and understanding the pathogenesis of endometriosis: a systematic review and meta-analysis 2024
- The Role of Peritoneal Immunity in Peritoneal Endometriosis and Related Infertility 2023
- Evidence Supporting the Diethylstilbestrol Induction of Endometriosis Via Immune-Inflammatory Pathway in Rat Model 2022
- Unveil the pain of endometriosis: from the perspective of the nervous system 2022
- Immunological Basis of the Endometriosis: The Complement System as a Potential Therapeutic Target 2021
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