ArticleThe Journal of experimental medicine2009
NF-kappaB activity marks cells engaged in receptor editing.
Article in The Journal of experimental medicine, 2009. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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.
The trial behind it
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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
24 citing papers in PubMed, 37 citations in OpenAlex.
- Inflammasome is a central player in B cell development and homing.Life science alliance · 2023Article
- Roles of interferon regulatory factor 4 in the AKI-CKD transition, glomerular diseases and kidney allograft rejection.Renal failure · 2023Review
- Asymmetrical forward and reverse developmental trajectories determine molecular programs of B cell antigen receptor editing.Science immunology · 2022Article
- Foxo3 Promotes Apoptosis of B Cell Receptor-Stimulated Immature B Cells, Thus Limiting the Window for Receptor Editing.Journal of immunology (Baltimore, Md. : 1950) · 2018Article
- Nuclear Factor-kappaB in Autoimmunity: Man and Mouse.Frontiers in immunology · 2018Review
- The value of detecting immunoglobulin gene rearrangements in the diagnosis of B-cell lymphoma.Oncotarget · 2017Article
- The Complex Interplay between DNA Injury and Repair in Enzymatically Induced Mutagenesis and DNA Damage in B Lymphocytes.International journal of molecular sciences · 2017Review
- Mechanisms of central tolerance for B cells.Nature reviews. Immunology · 2017Review
- Article
- Caspase-3 cleaved p65 fragment dampens NF-κB-mediated anti-apoptotic transcription by interfering with the p65/RPS3 interaction.FEBS letters · 2015Article
- Article
- Metalloprotease NleC suppresses host NF-κB/inflammatory responses by cleaving p65 and interfering with the p65/RPS3 interaction.PLoS pathogens · 2015Article
- IRF4 and IRF8: Governing the virtues of B Lymphocytes.Frontiers in biology · 2014Article
- Chronic lymphocytic leukaemia: could immunological tolerance mechanisms be the origin of lymphoid neoplasms?Immunology · 2014Review
- Phosphorothioate-modified CpG oligodeoxynucleotides mimic autoantigens and reveal a potential role for Toll-like receptor 9 in receptor revision.Immunology · 2013Article
- Sam68 modulates the promoter specificity of NF-κB and mediates expression of CD25 in activated T cells.Nature communications · 2013Article
- Identification of an N-terminal truncation of the NF-κB p65 subunit that specifically modulates ribosomal protein S3-dependent NF-κB gene expression.The Journal of biological chemistry · 2012Article
- Functionally Distinct Subpopulations of CpG-Activated Memory B Cells.Scientific reports · 2012Article
- Article
- Direct reduction of antigen receptor expression in polyclonal B cell populations developing in vivo results in light chain receptor editing.Journal of immunology (Baltimore, Md. : 1950) · 2012Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
6 authors at 3 institutions in 1 country.
Funding
Abstract
Because of the extreme diversity in immunoglobulin genes, tolerance mechanisms are necessary to ensure that B cells do not respond to self-antigens. One such tolerance mechanism is called receptor editing. If the B cell receptor (BCR) on an immature B cell recognizes self-antigen, it is down-regulated from the cell surface, and light chain gene rearrangement continues in an attempt to edit the autoreactive specificity. Analysis of a heterozygous mutant mouse in which the NF-kappaB-dependent IkappaB alpha gene was replaced with a lacZ (beta-gal) reporter complementary DNA (cDNA; IkappaB alpha(+/lacZ)) suggests a potential role for NF-kappaB in receptor editing. Sorted beta-gal(+) pre-B cells showed increased levels of various markers of receptor editing. In IkappaB alpha(+/lacZ) reporter mice expressing either innocuous or self-specific knocked in BCRs, beta-gal was preferentially expressed in pre-B cells from the mice with self-specific BCRs. Retroviral-mediated expression of a cDNA encoding an IkappaB alpha superrepressor in primary bone marrow cultures resulted in diminished germline kappa and rearranged lambda transcripts but similar levels of RAG expression as compared with controls. We found that IRF4 transcripts were up-regulated in beta-gal(+) pre-B cells. Because IRF4 is a target of NF-kappaB and is required for receptor editing, we suggest that NF-kappaB could be acting through IRF4 to regulate receptor editing.
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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.