4.5 Review

Insights into the role of complement system in the pathophysiology of endometriosis

Journal

IMMUNOLOGY LETTERS
Volume 231, Issue -, Pages 43-48

Publisher

ELSEVIER
DOI: 10.1016/j.imlet.2021.01.005

Keywords

Endometriosis; Complement system; Immunology; Biomarker; Therapeutic target

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Endometriosis is a gynecologic disorder affecting up to 10% of women in reproductive age, characterized by the presence of endometrium-like tissue outside of normal location. Research suggests dysfunction of the immune system, including the complement system, in endometriosis. Dysregulation of the complement system in endometriosis has been observed, with altered serum levels of complement proteins compared to non-affected individuals, indicating a potential role in the inflammatory pathogenesis of the disease.
Endometriosis (EM) is a gynecologic disorder characterized by the presence of endometrium-like tissue outside of normal location that affects up to 10 % of all women in reproductive age. The pathogenesis of endometriosis is not completely known. The relationship between complement and EM has already been demonstrated in some studies, indicating an important role in the pathophysiology of the disease, however, researches are scarce and sometimes controversial. The objective of this review is to bring state-of-the-art knowledge on the subject and promote better understanding of the complement system role in the pathophysiology of EM. We searched in databases up to December 2020 and found 1213 articles that were screened, from which were selected 54 articles from title and abstract. We found that there is a dysfunction of the immune system on endometriosis, including the complement system. Apparently, the complement system is dysregulated in endometriosis and several proteins of the three complement pathways presented serum levels altered in women with endometriosis compared with those without the disease. The most studied protein is C3. Future investigations on the innate immune response and complement system could offer a further understanding on the inflammatory pathogenesis of EM, which will support a new therapeutic plan.

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