Poly(I:C) stimulation upregulates HLA-G expression in human nasal epithelial cells.
TL;DR
Findings demonstrate HLA-G expression in HNECs and its upregulation by Poly(I:C), suggesting that HLA-G may be regulated in response to dsRNA-triggered innate immune signaling in the nasal epithelium.
Abstract
Human leukocyte antigen (HLA)-G is an immunosuppressive molecule involved in inflammation and has been reported to be induced by viral infections. Although the upper airway is a major entry site for viral pathogens, the expression of HLA-G in the nasal mucosa and its regulatory mechanisms remain unclear. We investigated HLA-G expression in primary human nasal epithelial cells (HNECs) and whether it is regulated by Toll-like receptor (TLR) stimulation. HNECs were stimulated with TLR1-9 agonists. HLA-G mRNA expression was quantified by reverse transcription quantitative polymerase chain reaction (RT-qPCR), and HLA-G protein expression was assessed by Western blotting. HLA-G mRNA was detected in unstimulated HNECs. Among the TLR agonists tested, TLR3 (polyinosinic-polycytidylic acid [Poly(I:C)]) stimulation significantly upregulated HLA-G mRNA expression (2.85-fold, 95% confidence interval 1.98-4.10). HLA-G mRNA expression increased with Poly(I:C) concentration, with significant upregulation at 1 and 10 μg/mL and a significant dose-response trend. At 10 μg/mL, mRNA expression was significantly upregulated from 16 h onward. Western blotting revealed that Poly(I:C) stimulation significantly upregulated HLA-G protein expression. These findings demonstrate HLA-G expression in HNECs and its upregulation by Poly(I:C), suggesting that HLA-G may be regulated in response to dsRNA-triggered innate immune signaling in the nasal epithelium.
