USP18 confers protection against allergic asthma by suppressing CCL8 production in alveolar type II epithelial cells.

ABSTRACT:

Background

Alveolar epithelial type II (AT2) cells participate in epithelial repair and lung immune defense, while the detailed molecular mechanisms through which AT2 cells regulate inflammatory immune responses in asthma remain unclear. Ubiquitin-specific peptidase 18 (USP18) has been implicated in immune regulation, but its role in asthma pathogenesis is not fully understood.

Methods

USP18 expression in AT2 cells was analyzed in both mouse models of allergic asthma and asthmatic patients. Functional studies were conducted using USP18 knockout mice, AT2 cell-specific chemokine (C-C motif) ligand 8 (CCL8) knockdown, and exogenous CCL8 treatment. Th2 responses, eosinophil recruitment, and chemokine production were assessed. Mechanistic investigations focused on USP18-mediated

SUBMITTER: Zhang H 

PROVIDER: S-EPMC12802203 | biostudies-literature | 2025 Dec

REPOSITORIES: biostudies-literature