An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.

<h4>Aims</h4>In the present study we have investigated the comparative switching propensity of murine peritoneal and splenic B cell subpopulations to IgA in presence of retinoic acid (RA) and TGF-β.<h4>Methods and results</h4>To study the influence of RA and TGF-β on switchin...

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Autores principales: Bishnudeo Roy, Anne-Margarete Brennecke, Shiwani Agarwal, Martina Krey, Sandra Düber, Siegfried Weiss
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Publicado: Public Library of Science (PLoS) 2013
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spelling oai:doaj.org-article:0f9dde417fac4792a8d5305ffa87dd822021-11-18T08:43:07ZAn intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.1932-620310.1371/journal.pone.0082121https://doaj.org/article/0f9dde417fac4792a8d5305ffa87dd822013-01-01T00:00:00Zhttps://www.ncbi.nlm.nih.gov/pmc/articles/pmid/24324757/?tool=EBIhttps://doaj.org/toc/1932-6203<h4>Aims</h4>In the present study we have investigated the comparative switching propensity of murine peritoneal and splenic B cell subpopulations to IgA in presence of retinoic acid (RA) and TGF-β.<h4>Methods and results</h4>To study the influence of RA and TGF-β on switching of B cell subpopulations to IgA, peritoneal (B1a, B1b and B2 cells) and splenic (B1a, marginal zone, and B2) B cells from normal BALB/c mice were FACS purified, cultured for 4 days in presence of RA and TGF-β and the number of IgA producing cells was determined by ELISPOT assay or FACS analysis. In presence of TGF-β, peritoneal B1b cells switched to IgA more potently than other peritoneal B cell subpopulations. When TGF-β was combined with retinoic acid (RA), switching to IgA was even more pronounced. Under these conditions, "innate" B cells like peritoneal and splenic B1 cells and MZ B cells produced IgA more readily than B2 cells. Additionally, high frequency of nucleotide exchanges indicating somatic hypermutation in VH regions was observed. Besides IgA induction, RA treatment of sorted PEC and splenic B cells led to expression of gut homing molecules - α4β7 and CCR9. Intraperitoneal transfer of RA-treated B1 cells into Rag1(-/-) recipients resulted in IgA in serum and gut lavage, most efficiently amongst B1b cell recipients.<h4>Conclusion</h4>Present study demonstrates the differential and synergistic effect of RA and TGF-β on switching of different B cell subpopulations to IgA and establishes the prominence of peritoneal B1b cells in switching to IgA under the influence of these two factors. Our study extends our knowledge about the existing differences among B cell subpopulations with regards to IgA production and indicates towards their differential contribution to gut associated humoral immunity.Bishnudeo RoyAnne-Margarete BrenneckeShiwani AgarwalMartina KreySandra DüberSiegfried WeissPublic Library of Science (PLoS)articleMedicineRScienceQENPLoS ONE, Vol 8, Iss 12, p e82121 (2013)
institution DOAJ
collection DOAJ
language EN
topic Medicine
R
Science
Q
spellingShingle Medicine
R
Science
Q
Bishnudeo Roy
Anne-Margarete Brennecke
Shiwani Agarwal
Martina Krey
Sandra Düber
Siegfried Weiss
An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
description <h4>Aims</h4>In the present study we have investigated the comparative switching propensity of murine peritoneal and splenic B cell subpopulations to IgA in presence of retinoic acid (RA) and TGF-β.<h4>Methods and results</h4>To study the influence of RA and TGF-β on switching of B cell subpopulations to IgA, peritoneal (B1a, B1b and B2 cells) and splenic (B1a, marginal zone, and B2) B cells from normal BALB/c mice were FACS purified, cultured for 4 days in presence of RA and TGF-β and the number of IgA producing cells was determined by ELISPOT assay or FACS analysis. In presence of TGF-β, peritoneal B1b cells switched to IgA more potently than other peritoneal B cell subpopulations. When TGF-β was combined with retinoic acid (RA), switching to IgA was even more pronounced. Under these conditions, "innate" B cells like peritoneal and splenic B1 cells and MZ B cells produced IgA more readily than B2 cells. Additionally, high frequency of nucleotide exchanges indicating somatic hypermutation in VH regions was observed. Besides IgA induction, RA treatment of sorted PEC and splenic B cells led to expression of gut homing molecules - α4β7 and CCR9. Intraperitoneal transfer of RA-treated B1 cells into Rag1(-/-) recipients resulted in IgA in serum and gut lavage, most efficiently amongst B1b cell recipients.<h4>Conclusion</h4>Present study demonstrates the differential and synergistic effect of RA and TGF-β on switching of different B cell subpopulations to IgA and establishes the prominence of peritoneal B1b cells in switching to IgA under the influence of these two factors. Our study extends our knowledge about the existing differences among B cell subpopulations with regards to IgA production and indicates towards their differential contribution to gut associated humoral immunity.
format article
author Bishnudeo Roy
Anne-Margarete Brennecke
Shiwani Agarwal
Martina Krey
Sandra Düber
Siegfried Weiss
author_facet Bishnudeo Roy
Anne-Margarete Brennecke
Shiwani Agarwal
Martina Krey
Sandra Düber
Siegfried Weiss
author_sort Bishnudeo Roy
title An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
title_short An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
title_full An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
title_fullStr An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
title_full_unstemmed An intrinsic propensity of murine peritoneal B1b cells to switch to IgA in presence of TGF-β and retinoic acid.
title_sort intrinsic propensity of murine peritoneal b1b cells to switch to iga in presence of tgf-β and retinoic acid.
publisher Public Library of Science (PLoS)
publishDate 2013
url https://doaj.org/article/0f9dde417fac4792a8d5305ffa87dd82
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