ArticleClinical immunology (Orlando, Fla.)2016
The BANK1 SLE-risk variants are associated with alterations in peripheral B cell signaling and development in humans.
Article in Clinical immunology (Orlando, Fla.), 2016. 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, 38 citations in OpenAlex.
- Identifying functional subtypes and common mechanisms of rheumatoid arthritis and systemic lupus erythematosus.Genes & diseases · 2025Article
- Article
- Bank1 modulates the differentiation and molecular profile of key B cell populations in autoimmunity.JCI insight · 2024Article
- Sequential immunotherapy: towards cures for autoimmunity.Nature reviews. Drug discovery · 2024Review
- Single-cell transcriptomic analysis of hematopoietic progenitor cells from patients with systemic lupus erythematosus reveals interferon-inducible reprogramming in early progenitors.Frontiers in immunology · 2024Article
- The Immunogenetics of Systemic Sclerosis.Advances in experimental medicine and biology · 2022Article
- Article
- Review
- Connection of BANK1, Tolerance, Regulatory B cells, and Apoptosis: Perspectives of a Reductionist Investigation.Frontiers in immunology · 2021Article
- BANK1 interacts with TRAF6 and MyD88 in innate immune signaling in B cells.Cellular & molecular immunology · 2020Article
- From Anti-EBV Immune Responses to the EBV Diseasome via Cross-reactivity.Global medical genetics · 2020Article
- Therapeutic implications of the anergic/postactivated status of B cells in systemic lupus erythematosus.RMD open · 2020Review
- Association ofFrontiers in genetics · 2020Article
- Driver gene alterations and activated signaling pathways toward malignant progression of gastrointestinal stromal tumors.Cancer science · 2019Article
- BLK and BANK1 polymorphisms and interactions are associated in Mexican patients with systemic lupus erythematosus.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2019Article
- Dynamic Immune Phenotypes of B and T Helper Cells Mark Distinct Stages of T1D Progression.Diabetes · 2019Article
- Exploring the etiopathogenesis of systemic lupus erythematosus: a genetic perspective.Immunogenetics · 2019Review
- The Post-GWAS Era: How to Validate the Contribution of Gene Variants in Lupus.Current rheumatology reports · 2019Review
- Identification and Characterization of Post-activated B Cells in Systemic Autoimmune Diseases.Frontiers in immunology · 2019Article
- Abnormal B Cell Development in Systemic Lupus Erythematosus: What the Genetics Tell Us.Arthritis & rheumatology (Hoboken, N.J.) · 2018Review
Corrections and comments
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
Abstract
Systemic lupus erythematosus (SLE) is a chronic autoimmune disease characterized by the development of autoantibodies that drive disease pathogenesis. Genetic studies have associated nonsynonymous variants in the BANK1 B cell scaffolding gene with susceptibility to SLE and autoantibodies in lupus. To determine how the BANK1 SLE-risk variants contribute to the dysregulated B cell program in lupus, we performed genotype/phenotype studies in human B cells. Targeted phospho-proteomics were used to evaluate BCR/CD40 signaling in human B cell lines engineered to express the BANK1 risk or non-risk variant proteins. We found that phosphorylation of proximal BCR signaling molecules was reduced in B cells expressing the BANK1 risk protein compared to the non-risk protein. Similar to these findings, we observed decreased B cell signaling in primary B cells from genotyped healthy control subjects carrying the BANK1 risk haplotype, including blunted BCR- and CD40-dependent AKT activation. Consistent with decreased AKT activation, we found that BANK1 risk B cells expressed increased basal levels of FOXO1 protein and increased expression of FOXO1 target genes upon stimulation compared to non-risk B cells. Healthy subjects carrying the BANK1 risk haplotype were also characterized by an expansion of memory B cells. Taken together, our results suggest that the SLE susceptibility variants in the BANK1 gene may contribute to lupus by altering B cell signaling, increasing FOXO1 levels, and enhancing memory B cell development.
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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 Socratic graph.