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CorrigendumImmunology Free access | 10.1172/JCI33760C1

APRIL secreted by neutrophils binds to heparan sulfate proteoglycans to create plasma cell niches in human mucosa

Bertrand Huard, Thomas McKee, Carine Bosshard, Stéphane Durual, Thomas Matthes, Samir Myit, Olivier Donze, Christophe Frossard, Carlo Chizzolini, Christiane Favre, Rudolf Zubler, Jean Philippe Guyot, Pascal Schneider, and Eddy Roosnek

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Published April 1, 2010 - More info

Published in Volume 120, Issue 4 on April 1, 2010
J Clin Invest. 2010;120(4):1362–1362. https://doi.org/10.1172/JCI33760C1.
© 2010 The American Society for Clinical Investigation
Published April 1, 2010 - Version history
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Related article:

APRIL secreted by neutrophils binds to heparan sulfate proteoglycans to create plasma cell niches in human mucosa
Bertrand Huard, … , Pascal Schneider, Eddy Roosnek
Bertrand Huard, … , Pascal Schneider, Eddy Roosnek
Research Article Immunology

APRIL secreted by neutrophils binds to heparan sulfate proteoglycans to create plasma cell niches in human mucosa

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Abstract

The bone marrow constitutes a favorable environment for long-lived antibody-secreting plasma cells, providing blood-circulating antibody. Plasma cells are also present in mucosa-associated lymphoid tissue (MALT) to mediate local frontline immunity, but how plasma cell survival there is regulated is not known. Here we report that a proliferation-inducing ligand (APRIL) promoted survival of human upper and lower MALT plasma cells by upregulating expression of the antiapoptotic proteins bcl-2, bcl-xL, and mcl-1. The in situ localization of APRIL was consistent with such a prosurvival role in MALT. In upper MALT, tonsillar epithelium produced APRIL. Upon infection, APRIL production increased considerably when APRIL-secreting neutrophils recruited from the blood infiltrated the crypt epithelium. Heparan sulfate proteoglycans (HSPGs) retained secreted APRIL in the subepithelium of the infected zone to create APRIL-rich niches, wherein IgG-producing plasma cells accumulated. In lower MALT, neutrophils were the unique source of APRIL, giving rise to similar niches for IgA-producing plasmocytes in villi of lamina propria. Furthermore, we found that mucosal humoral immunity in APRIL-deficient mice is less persistent than in WT mice. Hence, production of APRIL by inflammation-recruited neutrophils may create plasma cell niches in MALT to sustain a local antibody production.

Authors

Bertrand Huard, Thomas McKee, Carine Bosshard, Stéphane Durual, Thomas Matthes, Samir Myit, Olivier Donze, Christophe Frossard, Carlo Chizzolini, Christiane Favre, Rudolf Zubler, Jean Philippe Guyot, Pascal Schneider, Eddy Roosnek

×

Original citation: J. Clin. Invest.2008;118(8):2887–2895. doi:10.1172/JCI33760.

Citation for this corrigendum: J. Clin. Invest.2010;120(4):1362. doi:10.1172/JCI33760C1.

During the preparation of the manuscript, the reverse primer for qRT-PCR for the APRIL mRNA was given incorrectly. The correct sequence appears below.

5′-TCCCCTTGGTGTAAATGGAAGA-3′

The authors regret the errors.

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