Abstract
IFN-τ, a type I interferon produced by the trophoblasts of ruminants, has various important immune functions, including effects on the expression of major histocompatibility complex (MHC) class I (MHC-I). A previous study has reported that IFN-τ promotes the expression of MHC-I molecules on endometrial cells. However, the immunological mechanisms by which IFN-τ regulates MHC-I molecules remain unknown. Here, we investigated which microRNA (miRNAs) may be involved in the regulation of MHC-I molecule expression and function in bovine endometrial epithelial cells (bEECs). By using TargetScan 6.2 and http://www.microRNA.org, two miRNAs were suggested to target the 3′UTR of the bovine MHC-I heavy chain: bta-miR-148b and bta-miR-152. Dual luciferase reporter and miRNA mimic/inhibitor assays suggested that bta-miR-148b/152 were negatively correlated with bovine MHC-I heavy chain genes. The function of the MHC-I heavy chain was then investigated using qRT-PCR, ELISA, western blotting, immunofluorescence, and RNA interference assays in primary bEECs and an endometrial epithelial cell line (BEND). The results demonstrated that bta-miR-148b/152 could promote TLR4-triggered inflammatory responses by targeting the bovine MHC-I heavy chain, and the MHC-I molecule negatively regulated TLR4-induced inflammatory reactions may through the Fps-SHP-2 pathway. Our discovery offers novel insight into negative regulation of the TLR4 pathway and elucidates the mechanism by which bovine MHC-I molecules control congenital inflammatory reactions.
Highlights
IFN, a type I interferon, is secreted by ruminant animal trophoblasts [1]
We demonstrated that down-regulated bta-miR-148b/152 could suppress LPS-triggered inflammatory responses by targeting the bovine major histocompatibility complex (MHC)-I heavy chain, and the MHC class I (MHC-I) molecule negatively regulated TLR4-induced inflammatory reactions may through the Fps-SHP-2 pathway
The results showed that bta-miR-148b and bta-miR-152 expression was reduced, but the level of bovine MHC-I heavy chain mRNA was increased by IFN-τ treatment (Figure 1B)
Summary
IFN, a type I interferon, is secreted by ruminant animal trophoblasts [1]. It is responsible for maternal recognition of pregnancy in ruminants, which links the fields of developmental biology and reproductive immunology [2]. The bovine major histocompatibility complex (MHC), called the bovine leukocyte antigen (BoLA), is involved in the regulation of the immune response through antigen recognition by T lymphocytes [6]. Classical MHC-I molecules, such as the MHC-I heavy chain, play important roles in the immune bta-miR-148b/152 Impact Bovine MHC-I Expression response [8, 9]. Several studies have shown that IFN-τ promotes MHC-I expression on endometrial cells [10]. How the immunological mechanisms of IFN-τ regulate MHC-I molecules remains unknown. The high-throughput sequencing technology was employed to investigate the specific microRNA (miRNA) library of IFN-τ on bovine endometrial epithelial cells (bEECs) cells [11]
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