ArticleGenes and immunity2007
Expression of the autoimmune Fcgr2b NZW allele fails to be upregulated in germinal center B cells and is associated with increased IgG production.
Article in Genes and immunity, 2007. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 25 papers.
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Who cites it
25 citing papers in PubMed, 42 citations in OpenAlex.
- Pbx1 as a regulator of T-cell fate in autoimmunity.Frontiers in immunology · 2026Review
- Restoring B cell intrinsic tolerance to lupus autoimmunity: a rational strategy for lupus treatment.Frontiers in immunology · 2026Review
- Signaling Activation and Modulation in Extrafollicular B Cell Responses.Immunological reviews · 2025Review
- Immunosuppressive Polymeric Nanoparticles Targeting Dendritic Cells Alleviate Lupus Disease inInternational journal of molecular sciences · 2023Article
- FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation.The Journal of clinical investigation · 2022Article
- The Complex Association of FcγRIIb With Autoimmune Susceptibility.Frontiers in immunology · 2019Review
- Serologic features of cohorts with variable genetic risk for systemic lupus erythematosus.Molecular medicine (Cambridge, Mass.) · 2018Article
- Distinct and synergistic roles of FcγRIIB deficiency and 129 strain-derived SLAM family proteins in the development of spontaneous germinal centers and autoimmunity.Journal of autoimmunity · 2015Article
- Linking susceptibility genes and pathogenesis mechanisms using mouse models of systemic lupus erythematosus.Disease models & mechanisms · 2014Review
- Forward genetic approaches for elucidation of novel regulators of Lyme arthritis severity.Frontiers in cellular and infection microbiology · 2014Review
- Lupus Nephritis: Animal Modeling of a Complex Disease Syndrome Pathology.Drug discovery today. Disease models · 2014Article
- Analysis of a wild mouse promoter variant reveals a novel role for FcγRIIb in the control of the germinal center and autoimmunity.The Journal of experimental medicine · 2012Article
- Comprehensive gene expression profiling in the prefrontal cortex links immune activation and neutrophil infiltration to antinociception.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2012Article
- Activation-induced cytidine deaminase and aberrant germinal center selection in the development of humoral autoimmunities.The American journal of pathology · 2011Review
- Murine models of systemic lupus erythematosus.Journal of biomedicine & biotechnology · 2011Review
- Development of self-reactive germinal center B cells and plasma cells in autoimmune Fc gammaRIIB-deficient mice.The Journal of experimental medicine · 2010Article
- Murine lupus susceptibility locus Sle1a requires the expression of two sub-loci to induce inflammatory T cells.Genes and immunity · 2010Article
- Constitutive overexpression of BAFF in autoimmune-resistant mice drives only some aspects of systemic lupus erythematosus-like autoimmunity.Arthritis and rheumatism · 2010Article
- Genetics of SLE: evidence from mouse models.Nature reviews. Rheumatology · 2010Review
- Macrophages and immunologic inflammation of the kidney.Seminars in nephrology · 2010Review
Corrections and comments
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Authors and funding
6 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The inhibitory receptor FcgammaRIIb regulates B-cell functions. Genetic studies have associated Fcgr2b polymorphisms and lupus susceptibility in both humans and murine models, in which B cells express reduced FcgammaRIIb levels. Furthermore, FcgammaRIIb absence results in lupus on the appropriate genetic background, and lentiviral-mediated FcgammaRIIb overexpression prevents disease in the NZM2410 lupus mouse. The NZM2410/NZW allele Fcgr2b is, however, located in-between Sle1a and Sle1b, two potent susceptibility loci, making it difficult to evaluate Fcr2b(NZW) independent contribution. By using two congenic strains that each carries only Sle1a (B6.Sle1a(15-353)), or Fcr2b(NZW) in the absence of Sle1a or Sle1b (B6.Sle1(111-148)), we show that the Fcr2b(NZW) allele does not upregulate its expression on germinal center B cells and plasma cells, as does the C57BL/6 allele on B6.Sle1a(15-353) B cells. Furthermore, in the absence of the flanking Sle1a and Sle1b, Fcr2b(NZW) does not produce an autoimmune phenotype, but is associated with an increased number of class-switched plasma cells. These results show that while a lower level of FcgammaRIIb does not by itself induce the development of autoreactive B cells, it has the potential to amplify the contribution of autoreactive B cells induced by other lupus-susceptibility loci by enhancing the production of class-switched plasma cells.
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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.