Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ

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 and Adriana Gruppi ()
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Cristian Gabriel Beccaria: Universidad Nacional de Córdoba
María Carolina Amezcua Vesely: Universidad Nacional de Córdoba
Facundo Fiocca Vernengo: Universidad Nacional de Córdoba
Ricardo Carlos Gehrau: Universidad Nacional de Córdoba
María Cecilia Ramello: Universidad Nacional de Córdoba
Jimena Tosello Boari: Universidad Nacional de Córdoba
Melisa Gorosito Serrán: Universidad Nacional de Córdoba
Juan Mucci: Universidad Nacional de San Martín (UNSAM) - CONICET
Eliane Piaggio: INSERM U932
Oscar Campetella: Universidad Nacional de San Martín (UNSAM) - CONICET
Eva Virginia Acosta Rodríguez: Universidad Nacional de Córdoba
Carolina Lucía Montes: Universidad Nacional de Córdoba
Adriana Gruppi: Universidad Nacional de Córdoba

Nature Communications, 2018, vol. 9, issue 1, 1-15

Abstract: Abstract Germinal centers (GC) are important sites for high-affinity and long-lived antibody induction. Tight regulation of GC responses is critical for maintaining self-tolerance. Here, we show that Galectin-3 (Gal-3) is involved in GC development. Compared with WT mice, Gal-3 KO mice have more GC B cells and T follicular helper cells, increased percentages of antibody-secreting cells and higher concentrations of immunoglobulins and IFN-γ in serum, and develop a lupus-like disease. IFN-γ blockade in Gal-3 KO mice reduces spontaneous GC formation, class-switch recombination, autoantibody production and renal pathology, demonstrating that IFN-γ overproduction sustains autoimmunity. The results from chimeric mice show that intrinsic Gal-3 signaling in B cells controls spontaneous GC formation. Taken together, our data provide evidence that Gal-3 acts directly on B cells to regulate GC responses via IFN-γ and implicate the potential of Gal-3 as a therapeutic target in autoimmunity.

Date: 2018
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DOI: 10.1038/s41467-018-04063-5

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