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. 2023 May 12;14:1172641. doi: 10.3389/fimmu.2023.1172641

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Copyright © 2023 Wittner and Schuh

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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IgA plasmablast homing to the intestinal lamina propria (LP): Intestinal epithelial cells (IECs) express CCL25, which is presented on glucosamine-glycans on endothelial cells of venules as a ligand for the CCR9 receptor on IgA-expressing plasmablasts (and other immune cells). Integrin α4β7 is activated upon CCR9 signaling and binds to its ligand MadCAM-1, followed by plasmablast migration to the intestinal LP. Itgα4β7 and CCR9 expression is induced by KLF2 in IgA plasmablasts. Inside the LP, IgA plasmablasts differentiate into IgA-secreting plasma cells, a subset of those express ItgαEβ7 to localize close to the IECs. This mechanism might facilitate the binding of dimeric IgA to the poly-Ig receptor and might subsequently promote the transcytosis of dimeric IgA through the epithelial layer to the gut lumen. Itg, integrin; SIgA, secretory IgA.