Decrease in activated regulatory T cell populations in the endometrium during ovulation in endometriosis.


Journal

Journal of reproductive immunology
ISSN: 1872-7603
Titre abrégé: J Reprod Immunol
Pays: Ireland
ID NLM: 8001906

Informations de publication

Date de publication:
03 2023
Historique:
received: 16 11 2022
revised: 25 01 2023
accepted: 30 01 2023
pubmed: 10 2 2023
medline: 28 3 2023
entrez: 9 2 2023
Statut: ppublish

Résumé

Endometriosis is a serious disorder that can lead to infertility. The immune system, particularly regulatory T cells (Tregs), is involved in endometriosis and infertility; however, endometriosis-associated infertility is poorly understood. Tregs, which have an immunosuppressive function, fluctuate during the menstrual cycle. They are functionally heterogeneous and can be divided into subsets, with only activated Tregs (aTregs) having a true immunosuppressive function. The purpose of this study is to investigate the role of aTregs in endometriosis and how they contribute to endometriosis-associated infertility. We enrolled 72 women with (n = 39) and without (n = 33) endometriosis. Subpopulations of Tregs were examined in normal endometrium (NE), eutopic endometrium from women with endometriosis (EE), normal peritoneal fluid (N-PF), and peritoneal fluid from women with endometriosis (E-PF) via flow cytometry. The proportion of aTregs during the ovulatory phase was higher in NE than in EE (P < 0.05), and that during ovulatory and secretory phases was significantly higher in NE than in N-PF (P < 0.01 and 0.05, respectively). aTreg populations did not significantly differ between EE and E-PF. During the ovulatory phase, the proportion of resting Treg (rTreg) in the N-PF was significantly higher than during the proliferative phase (P < 0.05). The E-PF of rTreg populations did not differ significantly throughout the menstrual cycle. We found that Treg subsets were altered in the endometrium and PF of patients with endometriosis during the menstrual cycle. Our findings, particularly the reduction of aTregs in the EE, may provide an insight into the mechanism of endometriosis-associated infertility.

Identifiants

pubmed: 36758472
pii: S0165-0378(23)00031-1
doi: 10.1016/j.jri.2023.103825
pii:
doi:

Types de publication

Journal Article Research Support, Non-U.S. Gov't

Langues

eng

Sous-ensembles de citation

IM

Pagination

103825

Informations de copyright

Copyright © 2023 Elsevier B.V. All rights reserved.

Déclaration de conflit d'intérêts

Conflict of interest The authors have no competing interests to declare.

Auteurs

Maya Fujii (M)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Yukiko Tanaka (Y)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan. Electronic address: seki0818@koto.kpu-m.ac.jp.

Hiroyuki Okimura (H)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Eiko Maeda (E)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Masahide Hamaguchi (M)

Department of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Michiaki Fukui (M)

Department of Endocrinology and Metabolism, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Jo Kitawaki (J)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

Taisuke Mori (T)

Department of Obstetrics and Gynecology, Graduate School of Medical Science, Kyoto Prefectural University of Medicine, Kyoto 602-8566, Japan.

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Classifications MeSH