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Comment
. 2017 Apr 15;195(8):970-973.
doi: 10.1164/rccm.201612-2509ED.

A Hairline Crack in the Levee: Focal Secretory IgA Deficiency as a First Step toward Emphysema

Jeffrey L Curtis  1   2   3
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Comment

A Hairline Crack in the Levee: Focal Secretory IgA Deficiency as a First Step toward Emphysema

Jeffrey L Curtis. Am J Respir Crit Care Med. .
No abstract available

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Figures

Figure 1.
Figure 1.
Secretory immunoglobulin A (SIgA) secretion in small airways and its alteration in chronic obstructive pulmonary disease (COPD). (A) Structures of monomeric IgA versus SIgA. In serum, IgA principally circulates as IgA1 monomers, whereas SIgA is a dimer of two IgA monomers linked by J (“joining”) chain. SIgA is optimized to resist degradation at mucosal surfaces, both because its subunits are primarily IgA2 (which, relative to IgA1, possess a shorter hinge region that resists bacterial cleavage) and because the J chain protects portions of its structure. (B) In health, dimeric IgA (and pentameric IgM) are transcytosed across epithelial cells, from the basolateral surface into the mucosal lumen, by the polymeric Ig receptor (pIgR). Cleavage of pIgR at the luminal surface liberates SIgA, still bound to a portion of pIgR called the secretory component. SIgA prevents bacterial invasion of respiratory epithelium. (C) In COPD, pIgR is reduced, leading to localized SIgA deficiency in small airways (although not in larger airways where SIgA secretion directly via submucosal glands can compensate [13]). In the absence of SIgA, bacteria can invade respiratory epithelial cells. The resulting nuclear factor (NF)-κB activation initiates and sustains airway inflammation, setting the stage for development of centrilobular emphysema due to epithelial cell apoptosis. Artwork by Patricia Beals, adapted by permission from References and .
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