ArticleThe Journal of biological chemistry2014
Control of Toll-like receptor-mediated T cell-independent type 1 antibody responses by the inducible nuclear protein IκB-ζ.
Article in The Journal of biological chemistry, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 11 papers.
What it found
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Who cites it
11 citing papers in PubMed, 19 citations in OpenAlex.
- IκBζ target genes in chronic lymphocytic leukemia.iScience · 2026Article
- Functional Analysis of the Transcriptional Regulator IκB-ζ in Intestinal Homeostasis.Digestive diseases and sciences · 2022Article
- IgA natural antibodies are produced following T-cell independent B-cell activation following stroke.Brain, behavior, and immunity · 2021Article
- NF-κB and Its Regulators During Pregnancy.Frontiers in immunology · 2021Review
- The Curcumin Analog GO-Y030 Controls the Generation and Stability of Regulatory T Cells.Frontiers in immunology · 2021Article
- IκBζ facilitates protective immunity against Salmonella infection via Th1 differentiation and IgG production.Scientific reports · 2019Article
- Review
- Intra-CA1 Administration of Minocycline Alters the Expression of Inflammation-Related Genes in Hippocampus of CCI Rats.Frontiers in molecular neuroscience · 2019Article
- Toll-like receptor 9 stimulation can induce IκBζ expression and IgM secretion in chronic lymphocytic leukemia cells.Haematologica · 2017Article
- IκBζ: an emerging player in cancer.Oncotarget · 2016Review
- The atypical IκB protein IκB(NS) is important for Toll-like receptor-induced interleukin-10 production in B cells.Immunology · 2016Article
Corrections and comments
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Authors and funding
7 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antibody responses have been classified as being either T cell-dependent or T cell-independent (TI). TI antibody responses are further classified as being either type 1 (TI-1) or type 2 (TI-2), depending on their requirement for B cell-mediated antigen receptor signaling. Although the mechanistic basis of antibody responses has been studied extensively, it remains unclear whether different antibody responses share similarities in their transcriptional regulation. Here, we show that mice deficient in IκB-ζ, specifically in their B cells, have impaired TI-1 antibody responses but normal T cell-dependent and TI-2 antibody responses. The absence of IκB-ζ in B cells also impaired proliferation triggered by Toll-like receptor (TLR) activation, plasma cell differentiation, and class switch recombination (CSR). Mechanistically, IκB-ζ-deficient B cells could not induce TLR-mediated induction of activation-induced cytidine deaminase (AID), a class-switch DNA recombinase. Retroviral transduction of AID in IκB-ζ-deficient B cells restored CSR activity. Furthermore, acetylation of histone H3 in the vicinity of the transcription start site of the gene that encodes AID was reduced in IκB-ζ-deficient B cells relative to IκB-ζ-expressing B cells. These results indicate that IκB-ζ regulates TLR-mediated CSR by inducing AID. Moreover, IκB-ζ defines differences in the transcriptional regulation of different antibody responses.
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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 OpenQuestion graph.