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Impaired secretory IgA and mucosal immunity in cystic fibrosis: contribution to lung path
     
 
Author(s) : Pilette C, and De Rose V
Address : Université Catholique de Louvain, Brussels, Dip. di Scienze Biologiche e Cliniche, Università di Torino, Italy.
Université Catholique
info@postdocjournal.com

Background. Cystic fibrosis (CF) represents the most common lethal autosomal recessive disorder in the white population, mainly affecting the lungs. It affects the Cystic Fibrosis Transmembrane Regulator (CFTR) gene, which encodes a protein expressed on the apical membrane of airway epithelial cells, where it acts as a cAMP-dependent chloride channel and regulator of other channels, including the epithelial Na+ channel (ENaC). Airway colonization of the airways and lung infections are a hallmark of this disease, in particular with Pseudomonas aeruginosa (PA) that affects ~70% of CF patients and is associated with poor clinical outcomes. However, the mechanisms underlying the persistence of pathogens in CF airways, remain largely unclear. Secretory-immunoglobulin A (S-IgA) is a major line of mucosal defense, through so-called immune exclusion of inhaled / ingested antigens and pathogens. Following synthesis of polymeric (mainly dimeric) IgA by subepithelial mucosal plasma cells, IgA is transported across the epithelium by a transcellular routing mediated by the polymeric immunoglobulin receptor (pIgR). 

Hypothesis and objectives. This project aims to investigate whether the production of secretory IgA (S-IgA) is impaired in the CF lung, through which mechanisms, and whether this defect contributes to the pathogenesis of CF by impairing immunoprotection against respiratory pathogens such as PA. 

 
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