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

• DOI: 10.1038/s41467-018-04063-5
• Publication Date: 2018-04-18T11:42:15Z
• Authors: Cristian Gabriel ...; María Carolina Am...; Facundo Fiocca Ve...; Ricardo Carlos Ge...; María Cecilia Ram...; Jimena Tosello Boari; Melisa Gorosito S...; Juan Mucci; Eliane Piaggio; Oscar Campetella; Eva Virginia Acos...; Carolina Lucía Mo...; Adriana Gruppi
• Keywords: Galectin

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