Evaluation of Th17 and Treg cytokines in patients with unexplained recurrent pregnancy loss.

T helper 17 cells Tregs immunological responses unexplained recurrent pregnancy loss

Journal

Journal of clinical and translational research
ISSN: 2424-810X
Titre abrégé: J Clin Transl Res
Pays: Singapore
ID NLM: 101667205

Informations de publication

Date de publication:
29 Jun 2022
Historique:
received: 18 05 2021
revised: 28 11 2021
accepted: 07 04 2022
entrez: 11 7 2022
pubmed: 12 7 2022
medline: 12 7 2022
Statut: epublish

Résumé

The Th17/Treg balance in peripheral blood and reproductive tissues may have a role in the etiology of unexplained recurrent pregnancy loss (URPL). In this study, we evaluated the major cytokine of Treg cells transforming growth factor-beta (TGF-β), and their specific transcription factor Forkhead box P3 (FOXP3), as well as the most highlighted cytokine of Th17 cells (interleukin [IL]-17A) in both URPL patients and healthy women. Samples were extracted from the peripheral blood, endocervix, endometrium, and vagina of 14 patients with URPL and 12 normal non-pregnant women as a control (normal) group. Quantitative reverse transcription polymerase chain reaction was used to determine gene expression. Enzyme-linked immunosorbent assay was used to determine the levels of cytokines in the serum and cervicovaginal fluid. We found that in the URPL group, FOXP3 gene expression was considerably higher in peripheral blood than in the normal group ( Lower TGF-β levels in the cervicovaginal fluid of patients compared to controls may be related with increased IL-17 and FOXP3 mRNA levels in patients with URPL. Dysregulation of local immune responses in reproductive tissues may represent dysregulation of systemic regulatory immunological responses in the pathogenesis of URPL. Dysregulation of immune responses may play a role in the pathogenesis of URPL at least in some patients with URPL. We conclude that the breakdown of tolerance in the local immune responses is more critical than the breakdown of tolerance in systemic tolerance in the pathogenesis of URPL. Therefore, modulating immune responses in the endometrium and decidua may be the focus of future therapeutic approaches in URPL. The impact of seminal plasma on the expansion of Tregs may provide a novel therapeutic intervention that has already been used in assisted reproductive technologies. Therefore, we suggest that transvaginal TGF-β in women with URPL may induce maternal tolerance which leads to the successful pregnancy.

Sections du résumé

Background and Aim UNASSIGNED
The Th17/Treg balance in peripheral blood and reproductive tissues may have a role in the etiology of unexplained recurrent pregnancy loss (URPL). In this study, we evaluated the major cytokine of Treg cells transforming growth factor-beta (TGF-β), and their specific transcription factor Forkhead box P3 (FOXP3), as well as the most highlighted cytokine of Th17 cells (interleukin [IL]-17A) in both URPL patients and healthy women.
Methods UNASSIGNED
Samples were extracted from the peripheral blood, endocervix, endometrium, and vagina of 14 patients with URPL and 12 normal non-pregnant women as a control (normal) group. Quantitative reverse transcription polymerase chain reaction was used to determine gene expression. Enzyme-linked immunosorbent assay was used to determine the levels of cytokines in the serum and cervicovaginal fluid.
Results UNASSIGNED
We found that in the URPL group, FOXP3 gene expression was considerably higher in peripheral blood than in the normal group (
Conclusion UNASSIGNED
Lower TGF-β levels in the cervicovaginal fluid of patients compared to controls may be related with increased IL-17 and FOXP3 mRNA levels in patients with URPL. Dysregulation of local immune responses in reproductive tissues may represent dysregulation of systemic regulatory immunological responses in the pathogenesis of URPL.
Relevance for Patients UNASSIGNED
Dysregulation of immune responses may play a role in the pathogenesis of URPL at least in some patients with URPL. We conclude that the breakdown of tolerance in the local immune responses is more critical than the breakdown of tolerance in systemic tolerance in the pathogenesis of URPL. Therefore, modulating immune responses in the endometrium and decidua may be the focus of future therapeutic approaches in URPL. The impact of seminal plasma on the expansion of Tregs may provide a novel therapeutic intervention that has already been used in assisted reproductive technologies. Therefore, we suggest that transvaginal TGF-β in women with URPL may induce maternal tolerance which leads to the successful pregnancy.

Identifiants

pubmed: 35813894
pii: jctres.08.202203.001
pmc: PMC9260344

Types de publication

Journal Article

Langues

eng

Pagination

256-265

Informations de copyright

Copyright: © 2022 Whioce Publishing Pte. Ltd.

Déclaration de conflit d'intérêts

The authors declare no conflicts of interest. The authors alone are responsible for the content of this manuscript.

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Auteurs

Maral Farshchi (M)

Immunology Research Center, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran.

Elham Abdollahi (E)

Immunology Research Center, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran.
Department of Gynecology and Obstricts, Mashhad University of Medical Sciences, Mashhad, Iran.

Nafiseh Saghafi (N)

Department of Gynecology and Obstricts, Mashhad University of Medical Sciences, Mashhad, Iran.

Ahmad Hosseini (A)

Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran.

Sara Fallahi (S)

Shiraz IVF Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Sirus Rostami (S)

Shiraz IVF Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Parifar Rostami (P)

Shiraz IVF Center, Shiraz University of Medical Sciences, Shiraz, Iran.

Houshang Rafatpanah (H)

Immunology Research Center, Inflammation and Inflammatory Diseases Division, Mashhad University of Medical Sciences, Mashhad, Iran.

Mojtaba Habibagahi (M)

Department of Immunology, Shiraz University of Medical Sciences, Shiraz, Iran.

Classifications MeSH