ArticleImmunity2010
The ubiquitin modifying enzyme A20 restricts B cell survival and prevents autoimmunity.
Article in Immunity, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 166 papers, 3 of them syntheses that pooled it.
What it found
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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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Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
166 citing papers in PubMed, 3 syntheses or guidelines pooled it, 266 citations in OpenAlex.
- Three single nucleotide polymorphisms of TNFAIP3 gene increase the risk of rheumatoid arthritis.Oncotarget · 2017Pooled it
- Meta-analysis of the TNFAIP3 region in psoriasis reveals a risk haplotype that is distinct from other autoimmune diseases.Genes and immunity · 2015Pooled it
- Associations between TNFAIP3 gene polymorphisms and rheumatoid arthritis: a meta-analysis.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2012Pooled it
- The ubiquitin-editing enzyme A20 (TNFAIP3): mechanisms of activation, biological function, diseases and therapeutic targets.Molecular biomedicine · 2026Review
- TLR7 in systemic lupus erythematosus: genetics and emerging therapies.Nature reviews. Rheumatology · 2026Review
- Limitations of EBV transformed human Raji B cells as a model for measuring canonical NF-κB activation.bioRxiv : the preprint server for biology · 2026Article
- Article
- A20 Facilitates Oxaliplatin Sensitivity in Colorectal Cancer Through Monoubiquitylation of IKK-β.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Global trends and mechanistic insights into A20 (TNFAIP3) in autoimmunity and inflammation.American journal of translational research · 2026Review
- Monogenic disorders of the TNF signalling pathway.Nature reviews. Rheumatology · 2026Review
- Article
- Unrestrained MyD88 Signaling in A20-Deficient Keratinocytes Triggers T-Cell-Dependent Psoriatic Arthritis-Like Disease.The Journal of investigative dermatology · 2025Article
- A20 restriction of nitric oxide production restores macrophage bioenergetic balance.bioRxiv : the preprint server for biology · 2025Article
- Base-editing a single missense mutation in A20 enhances CAR-T cell efficacy.bioRxiv : the preprint server for biology · 2025Article
- Common origins of autoimmune diseases and lymphoid malignancies.Trends in immunology · 2025Review
- A20's linear ubiquitin-binding motif restrains pathogenic activation of Th17 cells and IL-22-driven enteritis.The Journal of clinical investigation · 2025Article
- Clinical features and genetic analysis of A20 haploinsufficiency.Orphanet journal of rare diseases · 2025Article
- The Role of A20 in Cancer: Friend or Foe?Cells · 2025Review
- A20 intrinsically influences human effector T-cell survival and function by regulating both NF-κB and JNK signaling.European journal of immunology · 2024Article
- A20 haploinsufficiency disturbs immune homeostasis and drives the transformation of lymphocytes with permissive antigen receptors.Science advances · 2024Article
106 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
11 authors at 2 institutions in 2 countries.
Funding
Abstract
A20 is a ubiquitin modifying enzyme that restricts NF-kappaB signals and protects cells against tumor necrosis factor (TNF)-induced programmed cell death. Given recent data linking A20 (TNFAIP3) with human B cell lymphomas and systemic lupus erythematosus (SLE), we have generated mice bearing a floxed allele of Tnfaip3 to interrogate A20's roles in regulating B cell functions. A20-deficient B cells are hyperresponsive to multiple stimuli and display exaggerated NF-kappaB responses to CD40-induced signals. Mice expressing absent or hypomorphic amounts of A20 in B cells possess elevated numbers of germinal center B cells, autoantibodies, and glomerular immunoglobulin deposits. A20-deficient B cells are resistant to Fas-mediated cell death, probably due to increased expression of NF-kappaB-dependent antiapoptotic proteins such as Bcl-x. These findings show that A20 can restrict B cell survival, whereas A20 protects other cells from TNF-induced cell death. Our studies demonstrate how reduced A20 expression predisposes to 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.