engleski

Expression and regulation of CD91 at the maternal fetal interface.

Heat shock protein 70 (HSP 70) is present in glandular epithelial cells and could be released during tissue remodeling at the maternal fetal-fetal interface of the first trimester normal pregnancy. It becomes forceful immunogen in the extracellular space and might compromise pregnancy. The aim of this study was to investigate the presence, distribution and regulation of CD91 receptor for HSP70 with specific progesterone mediator Progesterone Induced Blocking Factor (PIBF) in early pregnancy decidua. CD91+ cells with long extensions were found by immunohistology in the decidual stroma around the glands. Flow cytometry revealed the distribution of CD91 on NK cells and antigen presenting CD14+ macrophages, CD1a+ immature and CD83+ mature dendritic cells. T cells and NKT cells were CD91 negative. PIBF on a dose dependent manner decreased CD91 expression on mature CD83+ cells and cytotoxic CD56 dim+ NK subset, whereas it could not affect the expression of CD91 on immature CD1a+ cells and regulatory CD56 bright+ NK subset. Further, HSP 70 bound on CD91 on CD1a+ cells on a dose dependent manner, but it did not affect significantly their phenotype (CD80, CD86, CD83 and HLA-DR expression). Down-regulation of CD91 expression on activated decidual innate immune cells with PIBF contributes to the initiation of the immune response in normal early pregnancy decidua.

antigen presenting cells; CD91; dendritic cells; heat shock protein 70; NK cells; T cells; pregnancy; progesterone induced blocking factor

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