ArticleThe Journal of clinical investigation2022
FcγRIIB regulates autoantibody responses by limiting marginal zone B cell activation.
Article in The Journal of clinical investigation, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 28 citations in OpenAlex.
- B cell receptor signaling in autoimmune rheumatic diseases: regulatory mechanisms and therapeutic targeting.Frontiers in immunology · 2026Review
- Restoring B cell intrinsic tolerance to lupus autoimmunity: a rational strategy for lupus treatment.Frontiers in immunology · 2026Review
- A recombinant IgG1 Fc-domain protein ameliorates inflammatory demyelinating peripheral neuropathy.Frontiers in immunology · 2026Article
- Reduced vaccine-induced germinal center outputs in patients with inflammatory bowel disease treated with anti-TNF biologics.The Journal of clinical investigation · 2025Article
- The complement regulator CD55 modulates TLR9 signaling and supports survival in marginal zone B cells.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- 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
- Interferon signatures fuel B cell hyperactivity and plasmablast expansion in systemic lupus erythematosus.Journal of autoimmunity · 2025Article
- Circulating B cells display differential immune regulatory molecule expression in granulomatosis with polyangiitis.Clinical and experimental immunology · 2025Article
- Article
- Recent Advances in Biomimetic Drug Delivery for Rheumatoid Arthritis Treatment.International journal of nanomedicine · 2025Review
- Suppression of Pathological Allergen-Specific B Cells by Protein-Engineered Molecules in a Mouse Model of Chronic House Dust Mite Allergy.International journal of molecular sciences · 2024Article
- IFN-associated B cell hyperactivity is highly enriched in SLE patients harboring Sm/RNP antibodies.bioRxiv : the preprint server for biology · 2024Article
- Ro60-Roles in RNA Processing, Inflammation, and Rheumatic Autoimmune Diseases.International journal of molecular sciences · 2024Review
- FGL2/FcγRIIB Signalling Mediates Arterial Shear Stress-Mediated Endothelial Cell Apoptosis: Implications for Coronary Artery Bypass Vein Graft Pathogenesis.International journal of molecular sciences · 2024Article
- Antibody modulation of B cell responses-Incorporating positive and negative feedback.Immunity · 2024Review
- Vagus nerve stimulation modulates distinct acetylcholine receptors on B cells and limits the germinal center response.Science advances · 2024Article
- Elk1 enhances inflammatory cell infiltration and exacerbates acute lung injury/acute respiratory distress syndrome by suppressing Fcgr2b transcription.Molecular medicine (Cambridge, Mass.) · 2024Article
- Exercise Inhibits Doxorubicin-Induced Cardiotoxicity via Regulating B Cells.Circulation research · 2024Article
- B-Cell Immune Checkpoints Come of Age in Cardio-oncology.Circulation research · 2024Article
- Increased Immunoglobulin Gamma-3 Chain C in the Serum, Saliva, and Urine of Patients with Systemic Lupus Erythematosus.International journal of molecular sciences · 2023Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
FcγRIIB is an inhibitory receptor expressed throughout B cell development. Diminished expression or function is associated with lupus in mice and humans, in particular through an effect on autoantibody production and plasma cell (PC) differentiation. Here, we analyzed the effect of B cell-intrinsic FcγRIIB expression on B cell activation and PC differentiation. Loss of FcγRIIB on B cells in Fcgr2b-conditional KO (Fcgr2b-cKO) mice led to a spontaneous increase in autoantibody titers. This increase was most striking for IgG3, suggestive of increased extrafollicular responses. Marginal zone (MZ) B cells had the highest expression of FcγRIIB in both mice and humans. This high expression of FcγRIIB was linked to increased MZ B cell activation, Erk phosphorylation, and calcium flux in the absence of FcγRIIB triggering. We observed a marked increase in IgG3+ PCs and B cells during extrafollicular PC responses in Fcgr2b-cKO mice. The increased IgG3 response following immunization of Fcgr2b-cKO mice was lost in MZ-deficient Notch2 Fcgr2b-double KO mice. Importantly, patients with systemic lupus erythematosus (SLE) had a decrease in FcγRIIB expression that was strongest in MZ B cells. Thus, we present a model in which high FcγRIIB expression in MZ B cells prevented their hyperactivation and ensuing autoimmunity.
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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.