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. 2022 Dec 21;13:1076312. doi: 10.3389/fimmu.2022.1076312

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Copyright © 2022 Strugnell

This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms.

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Model for antigen excretion. (A) The pIgR serves to excrete antigen bound to dimeric IgA, reducing the sub-epithelial antigen burden. Antigen excretion can occur through polyspecific antibody from B-1 B-cells, but the efficiency of the excretion process is improved by the induction of specific IgA that occurs during e.g. infection. (B) In the absence of pIgR (or the secretable antibodies dIgA and pIgM), antigen accumulates in the sub-epithelial tissues. (C) The accumulation of infection- and microbiome-related PAMPs and antigen drives the infiltration of immune cells, increasing inflammation. (D) The cytokines produced by the inflammatory cells weakens the integrity of the epithelial barrier allowing ingress of bacteria from the lumen into the tissues, increasing inflammation further. The loss of epithelial patency also results in leakage of serum proteins including albumin into the lumen.