ArticleEuropean journal of immunology2013
FCRL3 promotes TLR9-induced B-cell activation and suppresses plasma cell differentiation.
Article in European journal of immunology, 2013. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 50 papers, 2 of them syntheses that pooled it.
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Who cites it
50 citing papers in PubMed, 2 syntheses or guidelines pooled it.
- Leveraging pleiotropy identifies common-variant associations with selective IgA deficiency.Clinical immunology (Orlando, Fla.) · 2024Pooled it
- Genome-Wide Meta-Analysis Identifies Three Novel Susceptibility Loci and Reveals Ethnic Heterogeneity of Genetic Susceptibility for IgA Nephropathy.Journal of the American Society of Nephrology : JASN · 2020Pooled it
- Genomic and transcriptomic correlates of Richter transformation in chronic lymphocytic leukemia.Blood · 2021Trial
- Identification of a systemic lupus erythematosus disease signature in resting naive B cells.The Journal of clinical investigation · 2026Article
- Progressive deterioration of adaptive immune repertoires in Down syndrome linked to interferon hyperactivity and lymphoid tissue disorganization.bioRxiv : the preprint server for biology · 2026Article
- Potential role of Akkermansia massiliensis in multiple sclerosis protection by the FcRL3 gene.Genes and immunity · 2026Article
- Integrating human plasma proteomes with genome-wide association data implicates novel proteins and drug targets for rheumatoid arthritis.Clinical proteomics · 2026Article
- FCRL3 as a potential link between Benzo[a]pyrene exposure and primary biliary cholangitis: insights from comparative toxicogenomics and multi-omics analysis.BMC gastroenterology · 2026Article
- FCRL3 is an immunoregulatory receptor that restrains the activation of human memory T lymphocytes.The Journal of experimental medicine · 2026Article
- Association ofFrontiers in bioinformatics · 2026Article
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- Plasmablast-like lymphoma cells as a distinct subpopulation confer multidrug resistance in PCNSL.Neuro-oncology · 2025Article
- Multivariate analysis of glycogenes reveals coordinated regulation of immunoglobulin glycosylation in an immortalized human B cell system.bioRxiv : the preprint server for biology · 2025Article
- Whole-Blood RNA Sequencing Profiling of Patients With Rheumatoid Arthritis Treated With Tofacitinib.ACR open rheumatology · 2025Article
- FcRL1, a New B-Cell-Activating Co-Receptor.International journal of molecular sciences · 2025Review
- RNAseq of peripheral blood mononucleated cells exposed to platelet-rich fibrin and enamel matrix derivatives.Scientific reports · 2025Article
- Revealing the key modules and potential prognostic markers of gastric cancer transformation based on weighted gene co-expression networks.Frontiers in genetics · 2025Article
- Evidence from a Comprehensive Bioinformatics Analysis Point to Possible Therapeutic Targets for Vitiligo.Clinical, cosmetic and investigational dermatology · 2025Article
- Integrated analyses of single-cell transcriptome and Mendelian randomization reveal the protective role of FCRL3 in multiple sclerosis.Frontiers in immunology · 2024Article
Corrections and comments
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Authors and funding
5 authors.
Funding
Abstract
Fc receptor-like (FCRL) molecules are preferentially expressed by B lymphocytes and possess tyrosine-based immunoregulatory function. Although they generally inhibit B-cell receptor signaling, their influence on other activation pathways remains largely unexplored. In humans, FCRL3 encodes a type I transmembrane protein harboring both cytoplasmic ITAM and ITIM elements that can repress B-cell receptor activation. Despite this inhibitory property, mounting associations for FCRL3 with autoimmune and lympho-proliferative disorders imply a role for it in promoting B-cell pathogenesis. Here, we explore the influence of FCRL3 on B-cell responses to innate TLR9 stimulation. A detailed survey of blood B-cell populations found that FCRL3 expression increased as a function of differentiation and was higher among memory subsets with innate-like features. FCRL3 ligation augmented CpG oligodeoxynucleotide TLR9-mediated B-cell proliferation, activation, and survival, but surprisingly, abrogated plasma cell differentiation and antibody production. Although FCRL3 amplified the NF-κB and mitogen-activated protein kinase signaling cascades, it halted CpG triggered BLIMP1 induction in an ERK-dependent fashion. These findings indicate that FCRL3 differentially modulates innate signaling in B cells and provide new insight into the potential of this disease-associated receptor to counter-regulate adaptive and innate immunity.
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Registered trials
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