NOX2-Deficient Pulmonary Neutrophils and Macrophages Have Lower PD-L1 Expression and May Aggravate Allergic Lung Inflammation through Affecting ILC Populations
نویسندگان
چکیده
Abstract Redox balance plays an important role in the pathogenesis of allergic asthma. We previously reported that NADPH oxidase 2 (NOX2)-derived ROS may modulate tissue inflammation through affecting neutrophil programmed cell death 1 ligand (PD-L1) expression. To reveal NOX2 regulating PD-L1 expressions on pulmonary neutrophils and macrophages ILC differentiation, we established asthma model using NOX2-deficient (Cybb−/−)mice stimulated with Dermatophagoides pteronyssinus(Der p) extract along LPS. first found deficiency led to increased group innate lymphoid (ILC2) Der p induced lung inflammation. The numbers neutrophil, eosinophil alveolar macrophage (AM) also Cybb−/−mice when compared WT mice. AM expressed higher levels CD11b M2 marker CD163 produced more TNF-α. Moreover, Cybb−/−neutrophils AMs had low while ILC2s significant (PD-1) expression inflammatory lungs. Altogether, these results indicated lead downregulation eliciting phenotype inducing amounts pro-inflammatory cytokine production. Our suggested lowered PDL1 aggravate Inflammation populations lung.
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ژورنال
عنوان ژورنال: Journal of Immunology
سال: 2023
ISSN: ['1550-6606', '0022-1767']
DOI: https://doi.org/10.4049/jimmunol.210.supp.67.07