We have located links that may give you full text access.
JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Placental trophoblasts shifted Th1/Th2 balance toward Th2 and inhibited Th17 immunity at fetomaternal interface.
The aims were to clarify the effect of placental trophoblasts on T lymphocytes by assessing production of cytokines and expression of transcription factors regulating Th1, Th2, and Th17 immunity in T lymphocytes. Placental trophoblasts were isolated and conditioned medium was made after trophoblast cultivation for 72 h. T lymphocytes were cultured in presence or absence of conditioned medium. ELISA was used to detect concentration of IL-2, TNF-α, IFN-γ, IL-4, IL-10, and IL-17 in supernatants of T cell and real-time PCR was used to detect the status of Th1 (T-bet, STAT-4), Th2 (GATA-3, STAT-6), and Th17 (RORC) immunity in T lymphocyte. We found that the level of IL-2, IFN-γ, TNF-α, and IL-17 was significantly decreased when T lymphocytes were cultured in conditioned medium compared with control, while IL-10 and IL-4 level were not significantly changed. The presence of conditioned medium significantly decreased the ratio of Th1/Th2. The expression of GATA-3 and STAT-6 were significantly increased and STAT-4 was reduced when T lymphocyte was cultured in conditioned medium, while the expression of T-bet and RORC was not significantly different. We concluded that placental trophoblast-induced shift of Th1/Th2 balance toward Th2 and inhibition of Th17 might be among the mechanisms involved in maternal tolerance to fetus.
Full text links
Related Resources
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app
All material on this website is protected by copyright, Copyright © 1994-2024 by WebMD LLC.
This website also contains material copyrighted by 3rd parties.
By using this service, you agree to our terms of use and privacy policy.
Your Privacy Choices
You can now claim free CME credits for this literature searchClaim now
Get seemless 1-tap access through your institution/university
For the best experience, use the Read mobile app