Correlation Engine 2.0
Clear Search sequence regions


Sizes of these terms reflect their relevance to your search.

Several lines of evidence strongly suggest that the contribution of human leukocyte antigen-G (HLA-G) and interleukin 10 receptor (IL10R) to maternal immunological tolerance toward paternal alloantigens of the embryo limits the activation and function of the maternal immune system. This study is aimed to assess the varia-tion of the mRNA expression levels of HLA-G and IL10RB genes in placental tissue of women with recurrent pregnancy loss (RPL). Placental tissue samples were collected from 78 women with a history of at least two consecutive miscarriages and 40 healthy women with no history of pregnancy loss. The expression of HLA-G and IL10RB in placental tissue specimens was evaluated by the quantitative real-time PCR (qPCR) method. Moreover, the correlation be-tween the expression levels of these genes and clinicopathological parameters was analyzed. The results showed that the expression of HLA-G was down-regulated in placental tissues samples of RPL patients compared to healthy subjects, while the expression of IL10RB was up-regulated, but none of them was statistically significant (p-value > 0.05). The mRNA expression levels of HLA-G and IL10RB in placental tissue of RPL patients were negatively correlated with age and number of miscarriages (p-value > 0.05). A significant positive correlation was observed between the expression levels of HLA-G and IL10RB in women with RPL (p-value < 0.05). The altered expression of HLA-G and IL10RB in placental tissue may contribute to the pathogenesis of RPL and therefore serve as potential therapeutic targets for its prevention.

Citation

Hourieh Khani, Mohammad A H Feizi, Reza Safaralizadeh, Jafar Mohseni, Mehdi Haghi. Altered Expression of the HLA-G and IL10RB Genes in Placental Tissue of Women with Recurrent Pregnancy Loss. Clinical laboratory. 2023 May 01;69(5)

Expand section icon Mesh Tags

Expand section icon Substances


PMID: 37145066

View Full Text