ArticleNature communications2018
Galectin-3 deficiency drives lupus-like disease by promoting spontaneous germinal centers formation via IFN-γ.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers, 1 of them a synthesis that pooled it.
What it found
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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
25 citing papers in PubMed, 1 synthesis or guideline pooled it, 53 citations in OpenAlex.
- Galectin-3 in systemic lupus erythematosus: a meta-analysis.Immunologic research · 2026Pooled it
- Galectin-3 restrains T cell-driven inflammation in the testis and epididymis.Cell death & disease · 2026Article
- Río Negro virus (Venezuelan equine encephalitis virus complex) shows pathogenic potential in a permissive murine model.Frontiers in cellular and infection microbiology · 2026Article
- The Role of Galectin-3 in Liver Inflammation and Fibrosis.Journal of inflammation research · 2026Review
- Adaptive resilience: agarikon mycelium modulates immune responses and provides oxidative stress buffering in human immune cells.Frontiers in immunology · 2026Article
- Follicular CD8+ T cells in Trypanosoma cruzi infection: helpers or killers depending on the target B cell population.PLoS pathogens · 2025Article
- Exploring the impact of galectins on liver cancer: From immunopathogenesis to potential targets.World journal of gastroenterology · 2025Review
- Galectin-8 deficiency promotes chronic splenomegaly persistence in Chagas disease.Frontiers in cellular and infection microbiology · 2025Article
- Sialic acid in the regulation of blood cell production, differentiation and turnover.Immunology · 2024Review
- Membrane organization by tetraspanins and galectins shapes lymphocyte function.Nature reviews. Immunology · 2024Review
- Immune regulatory networks coordinated by glycans and glycan-binding proteins in autoimmunity and infection.Cellular & molecular immunology · 2023Review
- TRAF3-EWSR1 signaling axis acts as a checkpoint on germinal center responses.The Journal of experimental medicine · 2023Article
- The role of galectins in immunity and infection.Nature reviews. Immunology · 2023Review
- Galectin-3 Mediates NETosis and Acts as an Autoantigen in Systemic Lupus Erythematosus-Associated Diffuse Alveolar Haemorrhage.International journal of molecular sciences · 2023Article
- Differential CpG DNA methylation of peripheral B cells, CD4Arthritis research & therapy · 2023Article
- Control of intestinal inflammation by glycosylation-dependent lectin-driven immunoregulatory circuits.Science advances · 2021Article
- The Role of Glycosylation in Inflammatory Diseases.Advances in experimental medicine and biology · 2021Article
- Quinoline-Pyrazole Scaffold as a Novel Ligand of Galectin-3 and Suppressor of TREM2 Signaling.ACS medicinal chemistry letters · 2020Article
- Human T cells employ conserved AU-rich elements to fine-tune IFN-γ production.European journal of immunology · 2020Article
- Suppression of age-related salivary gland autoimmunity by glycosylation-dependent galectin-1-driven immune inhibitory circuits.Proceedings of the National Academy of Sciences of the United States of America · 2020Article
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 2 countries.
Funding
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.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.