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Placental trophoblasts shifted Th1/Th2 balance toward Th2 and inhibited Th17 immunity at fetomaternal interface
Author(s) -
LIU FENGJUAN,
GUO JING,
TIAN TING,
WANG HANZHI,
DONG FANYI,
HUANG HEFENG,
DONG MINYUE
Publication year - 2011
Publication title -
apmis
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.909
H-Index - 88
eISSN - 1600-0463
pISSN - 0903-4641
DOI - 10.1111/j.1600-0463.2011.02774.x
Subject(s) - trophoblast , immunity , andrology , immunology , rar related orphan receptor gamma , interleukin 4 , placenta , chemistry , lymphocyte , biology , endocrinology , fetus , medicine , pregnancy , immune system , genetics , foxp3
Liu F, Guo J, Tian T, Wang H, Dong F, Huang H, Dong M. Placental trophoblasts shifted Th1/Th2 balance toward Th2 and inhibited Th17 immunity at fetomaternal interface. APMIS 2011. 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.