Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ
Germinal center (GC) is where B cells interact with other immune cells for optimal induction of antibody responses. Here the authors show that galectin-3 regulates GC development by modulating interferon-γ and B cell-intrinsic signaling, such that galectin-3 deficiency mice exhibit lupus-like autoim...
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Nature Portfolio
2018
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oai:doaj.org-article:e56f9c7562ff48e1b8ef2534da1247d22021-12-02T15:33:35ZGalectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ10.1038/s41467-018-04063-52041-1723https://doaj.org/article/e56f9c7562ff48e1b8ef2534da1247d22018-04-01T00:00:00Zhttps://doi.org/10.1038/s41467-018-04063-5https://doaj.org/toc/2041-1723Germinal center (GC) is where B cells interact with other immune cells for optimal induction of antibody responses. Here the authors show that galectin-3 regulates GC development by modulating interferon-γ and B cell-intrinsic signaling, such that galectin-3 deficiency mice exhibit lupus-like autoimmune symptoms.Cristian Gabriel BeccariaMaría Carolina Amezcua VeselyFacundo Fiocca VernengoRicardo Carlos GehrauMaría Cecilia RamelloJimena Tosello BoariMelisa Gorosito SerránJuan MucciEliane PiaggioOscar CampetellaEva Virginia Acosta RodríguezCarolina Lucía MontesAdriana GruppiNature PortfolioarticleScienceQENNature Communications, Vol 9, Iss 1, Pp 1-15 (2018) |
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Science Q Cristian Gabriel Beccaria María Carolina Amezcua Vesely Facundo Fiocca Vernengo Ricardo Carlos Gehrau María Cecilia Ramello Jimena Tosello Boari Melisa Gorosito Serrán Juan Mucci Eliane Piaggio Oscar Campetella Eva Virginia Acosta Rodríguez Carolina Lucía Montes Adriana Gruppi Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
description |
Germinal center (GC) is where B cells interact with other immune cells for optimal induction of antibody responses. Here the authors show that galectin-3 regulates GC development by modulating interferon-γ and B cell-intrinsic signaling, such that galectin-3 deficiency mice exhibit lupus-like autoimmune symptoms. |
format |
article |
author |
Cristian Gabriel Beccaria María Carolina Amezcua Vesely Facundo Fiocca Vernengo Ricardo Carlos Gehrau María Cecilia Ramello Jimena Tosello Boari Melisa Gorosito Serrán Juan Mucci Eliane Piaggio Oscar Campetella Eva Virginia Acosta Rodríguez Carolina Lucía Montes Adriana Gruppi |
author_facet |
Cristian Gabriel Beccaria María Carolina Amezcua Vesely Facundo Fiocca Vernengo Ricardo Carlos Gehrau María Cecilia Ramello Jimena Tosello Boari Melisa Gorosito Serrán Juan Mucci Eliane Piaggio Oscar Campetella Eva Virginia Acosta Rodríguez Carolina Lucía Montes Adriana Gruppi |
author_sort |
Cristian Gabriel Beccaria |
title |
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
title_short |
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
title_full |
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
title_fullStr |
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
title_full_unstemmed |
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ |
title_sort |
galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via ifn-γ |
publisher |
Nature Portfolio |
publishDate |
2018 |
url |
https://doaj.org/article/e56f9c7562ff48e1b8ef2534da1247d2 |
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