Deficient antiendometrium lymphocyte-mediated cytotoxicity in patients with endometriosis

P. Vigano, P. Vercellini, A. M. Di Blasio, A. Colombo, G. B. Candiani, M. Vignali

Research output: Contribution to journalArticlepeer-review

Abstract

Objective: To study the possible role of the immune system in the pathogenesis of endometriosis. Design: A cytotoxicity assay by 51Cr release was performed to determine the lymphocyte cytotoxic response toward endometrial targets and an erytroleukemic cell line (K562). Setting: The assays were performed in an academic research environment. Patients, Participants: Twenty-five control women and 25 patients with endometriosis were selected on the basis of laparoscopic examination. Interventions: The lymphocyte cytotoxic activity was evaluated separately on endometrial stromal and epithelial cells after 4 hours' incubation. Main Outcome Measure: The study was designed to determine, in controls and endometriosis patients, the lymphocyte-mediated cytotoxicity toward stromal and epithelial cells of endometrium. Results: The lymphocyte response in the presence of stromal cell antigens was significantly lower (P <0.02) in disease-affected women when compared with that obtained in controls (2.89 ± 0.87 and 7.64 ± 1.66, respectively). In contrast, when the same assay was performed on K562 cells, no difference was observed between endometriosis patients and controls. Conclusions: These data suggest that an alterated immune recognition might be one of the pathogenetic mechanisms of endometriosis. Moreover, they indicate that this is not a general phenomenon but is specific for the endometrial target.

Original languageEnglish
Pages (from-to)894-899
Number of pages6
JournalFertility and Sterility
Volume56
Issue number5
Publication statusPublished - 1991

ASJC Scopus subject areas

  • Obstetrics and Gynaecology

Fingerprint

Dive into the research topics of 'Deficient antiendometrium lymphocyte-mediated cytotoxicity in patients with endometriosis'. Together they form a unique fingerprint.

Cite this