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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Bibliographic Details
Main Authors: 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
Format: Article
Language:English
Published: Nature Publishing Group 2018-04-01
Series:Nature Communications
Online Access:https://doi.org/10.1038/s41467-018-04063-5
Description
Summary: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.
ISSN:2041-1723