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The Significance of Heat‐Shock Protein GP 96 and its Receptors' CD 91 and Toll‐Like Receptor 4 Expression at the Maternal Foetal Interface
Author(s) -
Gulic Tamara,
Laskarin Gordana,
Redzovic Arnela,
Eminović Senija,
Haller Herman,
Rukavina Daniel
Publication year - 2013
Publication title -
american journal of reproductive immunology
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.071
H-Index - 97
eISSN - 1600-0897
pISSN - 1046-7408
DOI - 10.1111/aji.12096
Subject(s) - decidua , trophoblast , placenta , receptor , biology , andrology , decidual cells , flow cytometry , pregnancy , microbiology and biotechnology , immunology , fetus , medicine , genetics
Problem 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. Results In missed abortion, gp96 was intensively stained, when compared to normal early pregnancy. The intensity of CD 91 and TLR 4 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 + , CD 91 + and TLR 4+ trophoblast. Progesterone‐induced blocking factor ( PIBF ) decreased the frequency of TLR 4 + T lymphocytes, CD 91 + T , natural killer ( NK ) and mature dendritic cells after an 18‐h culture. Decidual mononuclear cells ( DMC s) treated with PIBF down‐regulated CD 91, TLR 4 and gp96 gene expression. Conclusion The presence of gp96, CD 91 and TLR 4 at the maternal–foetal interface provides a molecular basis for their interaction, particularly in the absence of PIBF .