The Significance of Heat-Shock Protein GP96 and its Receptors' CD91 and Toll-Like Receptor 4 Expression at the Maternal Foetal Interface
Article first published online: 11 JUN 2013
© 2013 John Wiley & Sons Ltd
American Journal of Reproductive Immunology
Volume 70, Issue 1, pages 10–23, July 2013
How to Cite
The significance of heat-shock protein GP96 and its receptors' CD91 and toll-like receptor 4 expression at the maternal foetal interface. Am J Reprod Immunol 2013; 70: 10–23., , , , , .
- Issue published online: 11 JUN 2013
- Article first published online: 11 JUN 2013
- Manuscript Accepted: 19 JAN 2013
- Manuscript Received: 26 SEP 2012
- Croatian Ministry of Science
- Education and Sports. Grant Numbers: 0620402-0376, 0620402-0377, 062-620402-0379
- glycoprotein 96;
- maternal-fetal interface;
- progesterone-induced blocking factor;
- toll-like receptor 4
Differences in the expression of gp96 and its receptors were analysed in normal and pathological human pregnancy.
Material and Methods
Immunohistology and immunofluorescence of sections from decidual part of term placenta, first trimester normal decidua, missed abortion and blighted ovum decidua were performed together with reverse transcriptase–quantitative polymerase chain reaction and flow cytometry.
In missed abortion, gp96 was intensively stained, when compared to normal early pregnancy. The intensity of CD91 and TLR4 was higher in the first trimester pregnancy and blighted ovum, when compared to missed abortion. Decidual part of the term placenta is invaded with gp96+, CD91+ and TLR4+ trophoblast. Progesterone-induced blocking factor (PIBF) decreased the frequency of TLR4+ T lymphocytes, CD91+ T, natural killer (NK) and mature dendritic cells after an 18-h culture. Decidual mononuclear cells (DMCs) treated with PIBF down-regulated CD91, TLR4 and gp96 gene expression.
The presence of gp96, CD91 and TLR4 at the maternal–foetal interface provides a molecular basis for their interaction, particularly in the absence of PIBF.