ArticleImmunity, inflammation and disease2015
Overexpression of Fkbp11, a feature of lupus B cells, leads to B cell tolerance breakdown and initiates plasma cell differentiation.
Article in Immunity, inflammation and disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 19 papers, 1 of them a synthesis that pooled it.
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Who cites it
19 citing papers in PubMed, 1 synthesis or guideline pooled it, 28 citations in OpenAlex.
- The diversity of the plasmablast signature across species and experimental conditions: A meta-analysis.Immunology · 2021Pooled it
- Key RNA-binding proteins in renal fibrosis: a comprehensive bioinformatics and machine learning framework for diagnostic and therapeutic insights.Renal failure · 2025Article
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- G9a controls plasma cell differentiation through FOXO1 and ETS1 binding site regulatory networks.Journal of immunology (Baltimore, Md. : 1950) · 2025Article
- The prolyl isomerase FKBP11 is a secretory translocon accessory factor.Molecular biology of the cell · 2024Article
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- DnaJs are enriched in tau regulators.International journal of biological macromolecules · 2023Article
- Metagenomic and single-cell RNA-Seq survey of the Helicobacter pylori-infected stomach in asymptomatic individuals.JCI insight · 2023Article
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- Global discovery of lupus genetic risk variant allelic enhancer activity.Nature communications · 2021Article
- Immune Crosstalk Between Lymph Nodes and Breast Carcinomas, With a Focus on B Cells.Frontiers in molecular biosciences · 2021Review
- Single-cell analysis of germinal-center B cells informs on lymphoma cell of origin and outcome.The Journal of experimental medicine · 2020Article
- Identification and Development of a Novel 4-Gene Immune-Related Signature to Predict Osteosarcoma Prognosis.Frontiers in molecular biosciences · 2020Article
- FKBP11 protects intestinal epithelial cells against inflammation‑induced apoptosis via the JNK‑caspase pathway in Crohn's disease.Molecular medicine reports · 2018Article
- Trib1 Is Overexpressed in Systemic Lupus Erythematosus, While It Regulates Immunoglobulin Production in Murine B Cells.Frontiers in immunology · 2018Article
- Sex Differences in Correlation with Gene Expression Levels betweenJournal of immunology research · 2018Article
- Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017Review
- Weighted Gene Co-expression Network Analysis Identifies FKBP11 as a Key Regulator in Acute Aortic Dissection through a NF-kB Dependent Pathway.Frontiers in physiology · 2017Article
- PTPN22 inhibition resets defective human central B cell tolerance.Science immunology · 2016Article
Corrections and comments
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Authors and funding
12 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Systemic Lupus Erythematosus (SLE) is a severe systemic autoimmune disease, characterized by multi-organ damages, triggered by an autoantibody-mediated inflammation, and with a complex genetic influence. It is today accepted that adult SLE arises from the building up of many subtle gene variations, each one adding a new brick on the SLE susceptibility and contributing to a phenotypic trait to the disease. One of the ways to find these gene variations consists in comprehensive analysis of gene expression variation in a precise cell type, which can constitute a good complementary strategy to genome wide association studies. Using this strategy, and considering the central role of B cells in SLE, we analyzed the B cell transcriptome of quiescent SLE patients, and identified an overexpression of FKBP11, coding for a cytoplasmic putative peptidyl-prolyl cis/trans isomerase and chaperone enzyme. To understand the consequences of FKBP11 overexpression on B cell function and on autoimmunity's development, we created lentiviral transgenic mice reproducing this gene expression variation. We showed that high expression of Fkbp11 reproduces by itself two phenotypic traits of SLE in mice: breakdown of B cell tolerance against DNA and initiation of plasma cell differentiation by acting upstream of Pax5 master regulator gene.
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