ArticleThe Journal of experimental medicine2012
Analysis of a wild mouse promoter variant reveals a novel role for FcγRIIb in the control of the germinal center and autoimmunity.
Article in The Journal of experimental medicine, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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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
27 citing papers in PubMed, 43 citations in OpenAlex.
- Restoring B cell intrinsic tolerance to lupus autoimmunity: a rational strategy for lupus treatment.Frontiers in immunology · 2026Review
- The ETS-family transcription factor PU.1 is a critical regulator of the inhibitory Fcγ receptor IIB expression in humans.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- Signaling Activation and Modulation in Extrafollicular B Cell Responses.Immunological reviews · 2025Review
- Modulating Antigen Availability in Lymphoid Organs to Shape the Humoral Immune Response to Vaccines.Journal of immunology (Baltimore, Md. : 1950) · 2024Review
- FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation.The Journal of clinical investigation · 2022Article
- Two major genes associated with autoimmune arthritis, Ncf1 and Fcgr2b, additively protect mice by strengthening T cell tolerance.Cellular and molecular life sciences : CMLS · 2022Article
- Genetic dissection of a major haplotype associated with arthritis reveal FcγR2b and FcγR3 to act additively.European journal of immunology · 2021Article
- Article
- Leupaxin Expression Is Dispensable for B Cell Immune Responses.Frontiers in immunology · 2020Article
- B cell dissemination patterns during the germinal center reaction revealed by whole-organ imaging.The Journal of experimental medicine · 2019Article
- B Cell Fcγ Receptor IIb Modulates Atherosclerosis in Male and Female Mice by Controlling Adaptive Germinal Center and Innate B-1-Cell Responses.Arteriosclerosis, thrombosis, and vascular biology · 2019Article
- FcγRIIb differentially regulates pre-immune and germinal center B cell tolerance in mouse and human.Nature communications · 2019Article
- The Complex Association of FcγRIIb With Autoimmune Susceptibility.Frontiers in immunology · 2019Review
- Epistatic Interactions Between Mutations of Deoxyribonuclease 1-Like 3 and the Inhibitory Fc Gamma Receptor IIB Result in Very Early and Massive Autoantibodies Against Double-Stranded DNA.Frontiers in immunology · 2018Article
- Upregulation of FcγRIIB by resveratrol via NF-κB activation reduces B-cell numbers and ameliorates lupus.Experimental & molecular medicine · 2017Article
- Arthritis models: usefulness and interpretation.Seminars in immunopathology · 2017Review
- Spoiling for a Fight: B Lymphocytes As Initiator and Effector Populations within Tertiary Lymphoid Organs in Autoimmunity and Transplantation.Frontiers in immunology · 2017Review
- Germinal centers and autoimmune disease in humans and mice.Immunology and cell biology · 2016Review
- Review
- Reduced Atherosclerosis in apoE-inhibitory FcγRIIb-Deficient Mice Is Associated With Increased Anti-Inflammatory Responses by T Cells and Macrophages.Arteriosclerosis, thrombosis, and vascular biology · 2015Article
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Authors and funding
8 authors at 2 institutions in 2 countries.
Funding
Abstract
Genetic variants of the inhibitory Fc receptor FcγRIIb have been associated with systemic lupus erythematosus in humans and mice. The mechanism by which Fcgr2b variants contribute to the development of autoimmunity is unknown and was investigated by knocking in the most commonly conserved wild mouse Fcgr2b promoter haplotype, also associated with autoimmune-prone mouse strains, into the C57BL/6 background. We found that in the absence of an AP-1-binding site in its promoter, FcγRIIb failed to be up-regulated on activated and germinal center (GC) B cells. This resulted in enhanced GC responses, increased affinity maturation, and autoantibody production. Accordingly, in the absence of FcγRIIb activation-induced up-regulation, mice developed more severe collagen-induced arthritis and spontaneous glomerular immune complex deposition. Our data highlight how natural variation in Fcgr2b drives the development of autoimmune disease. They also show how the study of such variants using a knockin approach can provide insight into immune mechanisms not possible using conventional genetic manipulation, in this case demonstrating an unexpected critical role for the activation-induced up-regulation of FcγRIIb in controlling affinity maturation, autoantibody production, and 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.