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Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression

While TLR-activated pathways are key regulators of B cell responses in mammals, their impact on teleost B cells are scarcely addressed. Here, the potential of Atlantic salmon B cells to respond to TLR ligands was shown by demonstrating a constitutive expression of nucleic-acid sensing TLRs in magnet...

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Autores principales: Jenberie, Shiferaw, Thim, Hanna L., Sunyer, J. Oriol, Skjødt, Karsten, Jensen, Ingvill, Jørgensen, Jorunn B.
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Nature Publishing Group UK 2018
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824956/
https://www.ncbi.nlm.nih.gov/pubmed/29476080
http://dx.doi.org/10.1038/s41598-018-21895-9
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author Jenberie, Shiferaw
Thim, Hanna L.
Sunyer, J. Oriol
Skjødt, Karsten
Jensen, Ingvill
Jørgensen, Jorunn B.
author_facet Jenberie, Shiferaw
Thim, Hanna L.
Sunyer, J. Oriol
Skjødt, Karsten
Jensen, Ingvill
Jørgensen, Jorunn B.
author_sort Jenberie, Shiferaw
collection PubMed
description While TLR-activated pathways are key regulators of B cell responses in mammals, their impact on teleost B cells are scarcely addressed. Here, the potential of Atlantic salmon B cells to respond to TLR ligands was shown by demonstrating a constitutive expression of nucleic-acid sensing TLRs in magnetic sorted IgM(+) cells. Of the two receptors recognizing CpG in teleosts, tlr9 was the dominating receptor with over ten-fold higher expression than tlr21. Upon CpG-stimulation, IgM secretion increased for head kidney (HK) and splenic IgM(+) cells, while blood B cells were marginally affected. The results suggest that CpG directly affects salmon B cells to differentiate into antibody secreting cells (ASCs). IgM secretion was also detected in the non-treated controls, again with the highest levels in the HK derived population, signifying that persisting ASCs are present in this tissue. In all tissues, the IgM(+) cells expressed high MHCII levels, suggesting antigen-presenting functions. Upon CpG-treatment the co-stimulatory molecules cd83 and cd40 were upregulated, while cd86 was down-regulated under the same conditions. Finally, ifna1 was upregulated upon CpG-stimulation in all tissues, while a restricted upregulation was evident for ifnb, proposing that salmon IgM(+) B cells exhibit a type I IFN-response.
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spelling pubmed-58249562018-03-01 Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression Jenberie, Shiferaw Thim, Hanna L. Sunyer, J. Oriol Skjødt, Karsten Jensen, Ingvill Jørgensen, Jorunn B. Sci Rep Article While TLR-activated pathways are key regulators of B cell responses in mammals, their impact on teleost B cells are scarcely addressed. Here, the potential of Atlantic salmon B cells to respond to TLR ligands was shown by demonstrating a constitutive expression of nucleic-acid sensing TLRs in magnetic sorted IgM(+) cells. Of the two receptors recognizing CpG in teleosts, tlr9 was the dominating receptor with over ten-fold higher expression than tlr21. Upon CpG-stimulation, IgM secretion increased for head kidney (HK) and splenic IgM(+) cells, while blood B cells were marginally affected. The results suggest that CpG directly affects salmon B cells to differentiate into antibody secreting cells (ASCs). IgM secretion was also detected in the non-treated controls, again with the highest levels in the HK derived population, signifying that persisting ASCs are present in this tissue. In all tissues, the IgM(+) cells expressed high MHCII levels, suggesting antigen-presenting functions. Upon CpG-treatment the co-stimulatory molecules cd83 and cd40 were upregulated, while cd86 was down-regulated under the same conditions. Finally, ifna1 was upregulated upon CpG-stimulation in all tissues, while a restricted upregulation was evident for ifnb, proposing that salmon IgM(+) B cells exhibit a type I IFN-response. Nature Publishing Group UK 2018-02-23 /pmc/articles/PMC5824956/ /pubmed/29476080 http://dx.doi.org/10.1038/s41598-018-21895-9 Text en © The Author(s) 2018 Open Access This article is licensed under a Creative Commons Attribution 4.0 International License, which permits use, sharing, adaptation, distribution and reproduction in any medium or format, as long as you give appropriate credit to the original author(s) and the source, provide a link to the Creative Commons license, and indicate if changes were made. The images or other third party material in this article are included in the article’s Creative Commons license, unless indicated otherwise in a credit line to the material. If material is not included in the article’s Creative Commons license and your intended use is not permitted by statutory regulation or exceeds the permitted use, you will need to obtain permission directly from the copyright holder. To view a copy of this license, visit http://creativecommons.org/licenses/by/4.0/.
spellingShingle Article
Jenberie, Shiferaw
Thim, Hanna L.
Sunyer, J. Oriol
Skjødt, Karsten
Jensen, Ingvill
Jørgensen, Jorunn B.
Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title_full Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title_fullStr Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title_full_unstemmed Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title_short Profiling Atlantic salmon B cell populations: CpG-mediated TLR-ligation enhances IgM secretion and modulates immune gene expression
title_sort profiling atlantic salmon b cell populations: cpg-mediated tlr-ligation enhances igm secretion and modulates immune gene expression
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5824956/
https://www.ncbi.nlm.nih.gov/pubmed/29476080
http://dx.doi.org/10.1038/s41598-018-21895-9
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