This study investigates the role of the immunoproteasome subunit LMP7 in airway epithelial cells during rhinovirus (RV) infection. Using a tamoxifen-inducible, airway epithelial-specific LMP7 conditional Knockout (CKO) mouse model, the researchers demonstrated that LMP7 deficiency led to increased viral load, heightened neutrophilic inflammation, and reduced expression of the negative immune regulator A20/TNFAIP3. Additionally, induction of LMP7 via low-dose polyinosinic:polycytidylic acid (PI:C) treatment reduced RV-mediated inflammation, highlighting LMP7's protective role in antiviral and anti-inflammatory responses.
LMP7 in airway epithelial cells is crucial for resolving RV-induced lung inflammation and controlling viral replication. Its deficiency exacerbates inflammation and viral load, while its induction mitigates these effects, suggesting potential therapeutic avenues for RV infections.
Tamoxifen-inducible, airway epithelial-specific LMP7 conditional Knockout (CKO) mouse model, generated using Cre-loxP technology with Sox2-CreERT2 driver for targeted deletion of LMP7 in airway epithelial cells.
Rhinovirus infection, Airway inflammation, Immunoproteasome, LMP7, Antiviral immunity
Conditional Knockout model, Tamoxifen-inducible Cre-loxP system, Sox2-CreERT2 driver, Airway epithelial-specific gene deletion
From model design to experimental results
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