ArticleGlycobiology2013
Lack of galectin-1 or galectin-3 alters B cell deletion and anergy in an autoantibody transgene model.
Article in Glycobiology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 9 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
9 citing papers in PubMed, 16 citations in OpenAlex.
- Article
- Galectin-3 and prohibitin 1 are autoantigens in IgG4-related cholangitis without clear-cut protective effects against toxic bile acids.Frontiers in immunology · 2023Article
- Galectin-1 and Galectin-3 in B-Cell Precursor Acute Lymphoblastic Leukemia.International journal of molecular sciences · 2022Article
- Disruption of the preB Cell Receptor Complex Leads to Decreased Bone Mass.Frontiers in immunology · 2019Article
- Silica Exposure Differentially Modulates Autoimmunity in Lupus Strains and Autoantibody Transgenic Mice.Frontiers in immunology · 2019Article
- Galectin-3 deficiency enhances type 2 immune cell-mediated myocarditis in mice.Immunologic research · 2018Article
- Galectin-1 is required for the regulatory function of B cells.Scientific reports · 2018Article
- Galectin-Glycan Interactions as Regulators of B Cell Immunity.Frontiers in immunology · 2018Review
- Galectin-3 in autoimmunity and autoimmune diseases.Experimental biology and medicine (Maywood, N.J.) · 2015Review
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Members of the galectin family of proteins have been shown to regulate the development and the function of immune cells. We previously identified the increased expression of galectin-1 and galectin-3 mRNA and protein in anergic B cells relative to their naïve counterparts. To investigate the role of these galectins in maintaining B cell tolerance, we crossed mice deficient in galectin-1 or galectin-3 with mice bearing a lupus autoantigen-binding transgenic (Tg) B cell receptor, using a model with a well-characterized B cell tolerance phenotype of deletion, receptor editing and anergy. Here, we present data showing that the global knockout of galectin-1 or galectin-3 yields subtle alterations in B cell fate in autoantibody Tg mice. The absence of galectin-3 leads to a significant increase in the number of Tg spleen B cells, with the recovery of anti-laminin antibodies from a subset of mice. The B cell number increases further in antibody Tg mice with the dual deficiency of both galectin-1 and galectin-3. Isolated galectin-1 deficiency significantly enhances the proliferation of Tg B cells in response to lipopolysaccharide stimulation. These findings add to the growing body of evidence indicating a role for the various galectin family members, and for galectins 1 and 3 in particular, in the regulation of 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.