The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.

It is currently unknown how mucosal adjuvants cause induction of secretory immunoglobulin A (IgA), and how T cell-dependent (TD) or -independent (TI) pathways might be involved. Mucosal dendritic cells (DCs) are the primary antigen presenting cells driving TI IgA synthesis, by producing a proliferat...

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Autores principales:	Anouk K Gloudemans, Maud Plantinga, Martin Guilliams, Monique A Willart, Arifa Ozir-Fazalalikhan, Alwin van der Ham, Louis Boon, Nicola L Harris, Hamida Hammad, Henk C Hoogsteden, Maria Yazdanbakhsh, Rudi W Hendriks, Bart N Lambrecht, Hermelijn H Smits
Formato:	article
Lenguaje:	EN
Publicado:	Public Library of Science (PLoS) 2013
Materias:	Medicine R Science Q
Acceso en línea:	https://doaj.org/article/cee7ddb13e3e45cfbe33652d910078eb
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spelling	oai:doaj.org-article:cee7ddb13e3e45cfbe33652d910078eb2021-11-18T07:52:35ZThe mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.1932-620310.1371/journal.pone.0059822https://doaj.org/article/cee7ddb13e3e45cfbe33652d910078eb2013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/23527272/pdf/?tool=EBIhttps://doaj.org/toc/1932-6203It is currently unknown how mucosal adjuvants cause induction of secretory immunoglobulin A (IgA), and how T cell-dependent (TD) or -independent (TI) pathways might be involved. Mucosal dendritic cells (DCs) are the primary antigen presenting cells driving TI IgA synthesis, by producing a proliferation-inducing ligand (APRIL), B cell activating factor (BAFF), Retinoic Acid (RA), TGF-β or nitric oxide (NO). We hypothesized that the mucosal adjuvant Cholera Toxin subunit B (CTB) could imprint non-mucosal DCs to induce IgA synthesis, and studied the mechanism of its induction. In vitro, CTB-treated bone marrow derived DCs primed for IgA production by B cells without the help of T cells, yet required co-signaling by different Toll-like receptor (TLR) ligands acting via the MyD88 pathway. CTB-DC induced IgA production was blocked in vitro or in vivo when RA receptor antagonist, TGF-β signaling inhibitor or neutralizing anti-TGF-β was added, demonstrating the involvement of RA and TGF-β in promoting IgA responses. There was no major involvement for BAFF, APRIL or NO. This study highlights that synergism between CTB and MyD88-dependent TLR signals selectively imprints a TI IgA-inducing capacity in non-mucosal DCs, explaining how CTB acts as an IgA promoting adjuvant.Anouk K GloudemansMaud PlantingaMartin GuilliamsMonique A WillartArifa Ozir-FazalalikhanAlwin van der HamLouis BoonNicola L HarrisHamida HammadHenk C HoogstedenMaria YazdanbakhshRudi W HendriksBart N LambrechtHermelijn H SmitsPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 3, p e59822 (2013)
institution	DOAJ
collection	DOAJ
language	EN
topic	Medicine R Science Q
spellingShingle	Medicine R Science Q Anouk K Gloudemans Maud Plantinga Martin Guilliams Monique A Willart Arifa Ozir-Fazalalikhan Alwin van der Ham Louis Boon Nicola L Harris Hamida Hammad Henk C Hoogsteden Maria Yazdanbakhsh Rudi W Hendriks Bart N Lambrecht Hermelijn H Smits The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
description	It is currently unknown how mucosal adjuvants cause induction of secretory immunoglobulin A (IgA), and how T cell-dependent (TD) or -independent (TI) pathways might be involved. Mucosal dendritic cells (DCs) are the primary antigen presenting cells driving TI IgA synthesis, by producing a proliferation-inducing ligand (APRIL), B cell activating factor (BAFF), Retinoic Acid (RA), TGF-β or nitric oxide (NO). We hypothesized that the mucosal adjuvant Cholera Toxin subunit B (CTB) could imprint non-mucosal DCs to induce IgA synthesis, and studied the mechanism of its induction. In vitro, CTB-treated bone marrow derived DCs primed for IgA production by B cells without the help of T cells, yet required co-signaling by different Toll-like receptor (TLR) ligands acting via the MyD88 pathway. CTB-DC induced IgA production was blocked in vitro or in vivo when RA receptor antagonist, TGF-β signaling inhibitor or neutralizing anti-TGF-β was added, demonstrating the involvement of RA and TGF-β in promoting IgA responses. There was no major involvement for BAFF, APRIL or NO. This study highlights that synergism between CTB and MyD88-dependent TLR signals selectively imprints a TI IgA-inducing capacity in non-mucosal DCs, explaining how CTB acts as an IgA promoting adjuvant.
format	article
author	Anouk K Gloudemans Maud Plantinga Martin Guilliams Monique A Willart Arifa Ozir-Fazalalikhan Alwin van der Ham Louis Boon Nicola L Harris Hamida Hammad Henk C Hoogsteden Maria Yazdanbakhsh Rudi W Hendriks Bart N Lambrecht Hermelijn H Smits
author_facet	Anouk K Gloudemans Maud Plantinga Martin Guilliams Monique A Willart Arifa Ozir-Fazalalikhan Alwin van der Ham Louis Boon Nicola L Harris Hamida Hammad Henk C Hoogsteden Maria Yazdanbakhsh Rudi W Hendriks Bart N Lambrecht Hermelijn H Smits
author_sort	Anouk K Gloudemans
title	The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
title_short	The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
title_full	The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
title_fullStr	The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
title_full_unstemmed	The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.
title_sort	mucosal adjuvant cholera toxin b instructs non-mucosal dendritic cells to promote iga production via retinoic acid and tgf-β.
publisher	Public Library of Science (PLoS)
publishDate	2013
url	https://doaj.org/article/cee7ddb13e3e45cfbe33652d910078eb
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The mucosal adjuvant cholera toxin B instructs non-mucosal dendritic cells to promote IgA production via retinoic acid and TGF-β.

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