ArticleToxicology and applied pharmacology2011
2,3,7,8-Tetrachlorodibenzo-p-dioxin-mediated disruption of the CD40 ligand-induced activation of primary human B cells.
Article in Toxicology and applied pharmacology, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 22 papers.
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Who cites it
22 citing papers in PubMed, 32 citations in OpenAlex.
- Using the Key Characteristics Framework to Unlock the Mysteries of Aryl Hydrocarbon Receptor-Mediated Effects on the Immune System.Annual review of immunology · 2025Review
- Evolutive emergence and divergence of an Ig regulatory node: An environmental sensor getting cues from the aryl hydrocarbon receptor?Frontiers in immunology · 2023Review
- Role of Programmed Cell Death Protein-1 and Lymphocyte Specific Protein Tyrosine Kinase in the Aryl Hydrocarbon Receptor- Mediated Impairment of the IgM Response in Human CD5Frontiers in immunology · 2022Article
- TCDD attenuates EAE through induction of FasL on B cells and inhibition of IgG production.Toxicology · 2021Article
- Identification of a Sensitive Human Immunological Target of Aryl Hydrocarbon Receptor Activation: CD5Frontiers in immunology · 2021Article
- TCDD-mediated suppression of naïve human B cell IgM secretion involves aryl hydrocarbon receptor-mediated reduction in STAT3 serine 727 phosphorylation and is restored by interferon-γ.Cellular signalling · 2020Article
- Embracing Systems Toxicology at Single-Cell Resolution.Current opinion in toxicology · 2019Article
- Sphingomyelin synthase 1 enhances BCR signaling to promote lupus-like autoimmune response.EBioMedicine · 2019Article
- Characterizing Serpinb2 as a Modulator of TCDD-Induced Suppression of the B Cell.Chemical research in toxicology · 2018Article
- Lymphocyte-Specific Protein Tyrosine Kinase (LCK) is Involved in the Aryl Hydrocarbon Receptor-Mediated Impairment of Immunoglobulin Secretion in Human Primary B Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Suppression of the IgM Response by Aryl Hydrocarbon Receptor Activation in Human Primary B Cells Involves Impairment of Immunoglobulin Secretory Processes.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Aryl Hydrocarbon Receptor Activation Suppresses EBF1 and PAX5 and Impairs Human B Lymphopoiesis.Journal of immunology (Baltimore, Md. : 1950) · 2017Article
- Aryl hydrocarbon receptor activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin impairs human B lymphopoiesis.Toxicology · 2017Article
- Comparative analysis of TCDD-induced AhR-mediated gene expression in human, mouse and rat primary B cells.Toxicology and applied pharmacology · 2017Article
- SHP-1 is directly activated by the aryl hydrocarbon receptor and regulates BCL-6 in the presence of 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD).Toxicology and applied pharmacology · 2016Article
- The Influence of Human Interindividual Variability on the Low-Dose Region of Dose-Response Curve Induced by 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in Primary B Cells.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Suppression of human B cell activation by 2,3,7,8-tetrachlorodibenzo-p-dioxin involves altered regulation of B cell lymphoma-6.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
- Article
- Autoimmunity and infection in Sjögren's syndrome.Current opinion in rheumatology · 2013Review
- Comparative analysis of temporal and dose-dependent TCDD-elicited gene expression in human, mouse, and rat primary hepatocytes.Toxicological sciences : an official journal of the Society of Toxicology · 2013Article
Corrections and comments
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Authors and funding
4 authors at 1 institution in 1 country.
Funding
Abstract
Suppression of the primary antibody response is particularly sensitive to suppression by 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) in mice; however, surprisingly little is known concerning the effects of TCDD on humoral immunity or B cell function in humans. Results from a limited number of previous studies, primarily employing in vitro activation models, suggested that human B cell effector function is suppressed by TCDD. The present study sought to extend these findings by investigating, in primary human B cells, the effects of TCDD on several critical stages leading to antibody secretion including activation and plasmacytic differentiation using an in vitro CD40 ligand activation model. These studies revealed important differences in the response of human and mouse B cells to TCDD, the most striking being altered expression of plasmacytic differentiation regulators, B lymphocyte-induced maturation protein 1 and paired box protein 5, in mouse but not human B cells. The activation of human B cells was profoundly impaired by TCDD, as evidenced by decreased expression of activation markers CD80, CD86, and CD69. The impaired activation correlated with decreased cell viability, which prevented the progression of human B cells toward plasmacytic differentiation. TCDD treatment also attenuated the early activation of mitogen-activated protein kinases (MAPK) and Akt signaling in human B cells. Collectively, the present study provided experimental evidence for novel mechanisms by which TCDD impairs the effector function of primary human B cells.
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Registered trials
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