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Progesterone Decreases in vitro Indoleamine 2, 3-dioxygenase Expression in Dendritic and CD4 + Cells from Maternal-Fetal Interface of Rats.

Authors :
Bianchi PKFDC
Leandro RM
Poscai AN
Yoshinaga T
Gonçalez PO
Kfoury Junior JR
Source :
Immunological investigations [Immunol Invest] 2017 Jul; Vol. 46 (5), pp. 447-459. Date of Electronic Publication: 2017 Apr 17.
Publication Year :
2017

Abstract

Problem: Several mechanisms contribute to the tolerogenic state observed during pregnancy, such as the activity of the enzyme indoleamine 2, 3-dioxygenase (IDO). This initializes the catabolism of tryptophan, inducing T cells to apoptosis due to its deprivation and by the action of its catabolites in the placental microenvironment. Progesterone plays an important part on immunological tolerance mechanisms during pregnancy; however, there is no evidence it is related to IDO activity. Thus, this study aimed to investigate progesterone influence on the maternal-fetal interface of pregnant Wistar rats, by identifying IDO positive cells by immunophenotyping and flow cytometry under exogenous progesterone supplementation.<br />Method of Study: Placenta and embryo cells were cultured and separated into groups that received interferon γ or progesterone, supplemented or not with mifepristone. After 2 and 24 h, these were labeled with an anti-IDO and a series of antibodies specific to leucocytes and progesterone receptor and processed through flow cytometry analysis.<br />Results: Progesterone induced a significant decrease in the expression of IDO in dendritic cells and CD4 <superscript>+</superscript> lymphocytes.<br />Conclusion: The blocking of progesterone receptor on these cells by mifepristone restored IDO expression levels and may constitute evidence of the participation of this hormone through a direct route in these cells.

Details

Language :
English
ISSN :
1532-4311
Volume :
46
Issue :
5
Database :
MEDLINE
Journal :
Immunological investigations
Publication Type :
Academic Journal
Accession number :
28414589
Full Text :
https://doi.org/10.1080/08820139.2017.1296856