ArticleEnvironmental health perspectives2011
Gene expression alterations in immune system pathways in the thymus after exposure to immunosuppressive chemicals.
Article in Environmental health perspectives, 2011. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 48 citations in OpenAlex.
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- HPTE-Induced Embryonic Thymocyte Death and Alteration of Differentiation Is Not Rescued by ERα or GPER Inhibition but Is Exacerbated by Concurrent TCR Signaling.International journal of molecular sciences · 2021Article
- In utero exposure to genistein decreased intranasal house dust mite-induced respiratory allergy in middle-aged male B6C3F1 offspring.Toxicology letters · 2020Article
- Methoxychlor metabolite HPTE alters viability and differentiation of embryonic thymocytes from C57BL/6 mice.Journal of immunotoxicology · 2018Article
- Thymic function in the regulation of T cells, and molecular mechanisms underlying the modulation of cytokines and stress signaling (Review).Molecular medicine reports · 2017Review
- Immunotoxicology: A brief history, current status and strategies for future immunotoxicity assessment.Current opinion in toxicology · 2017Article
- In Utero exposure to genistein enhanced intranasal house dust mite allergen-induced respiratory sensitization in young adult B6C3F1 mice.Toxicology letters · 2016Article
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- Human Peripheral Blood Mononuclear Cell Function and Dendritic Cell Differentiation Are Affected by Bisphenol-A Exposure.PloS one · 2016Article
- Exposure to diethylstilbestrol during pregnancy modulates microRNA expression profile in mothers and fetuses reflecting oncogenic and immunological changes.Molecular pharmacology · 2015Article
- Genistein modulation of streptozotocin diabetes in male B6C3F1 mice can be induced by diet.Toxicology and applied pharmacology · 2014Article
- Relative potency for altered humoral immunity induced by polybrominated and polychlorinated dioxins/furans in female B6C3F1/N mice.Toxicological sciences : an official journal of the Society of Toxicology · 2014Article
- Preventive effect of pidotimod on reactivated toxoplasmosis in mice.Parasitology research · 2013Article
- Molecular mechanism(s) of endocrine-disrupting chemicals and their potent oestrogenicity in diverse cells and tissues that express oestrogen receptors.Journal of cellular and molecular medicine · 2013Review
- Article
- Prenatal exposure of mice to diethylstilbestrol disrupts T-cell differentiation by regulating Fas/Fas ligand expression through estrogen receptor element and nuclear factor-κB motifs.The Journal of pharmacology and experimental therapeutics · 2012Article
- Toxicogenomic profiles in relation to maternal immunotoxic exposure and immune functionality in newborns.Toxicological sciences : an official journal of the Society of Toxicology · 2012Article
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Authors and funding
6 authors at 2 institutions in 1 country.
Funding
Abstract
backgroundDysregulation of positive and negative selection, antigen presentation, or apoptosis in the thymus can lead to immunosuppression or autoimmunity. Diethylstilbestrol (DES), dexamethasone (DEX), cyclophosphamide (CPS), and 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD) are immunosuppressive chemicals that induce similar immunotoxic effects in the thymus, however, the mechanism of toxicity is purported to be different for each compound.
objectivesWe hypothesized that genomic analysis of thymus after chemical-induced atrophy would yield transcriptional profiles that suggest pathways of toxicity associated with reduced function.
methodsFemale B6C3F1 mice were exposed to these immunosuppressive agents and changes in gene expression and immune cell subpopulations were evaluated.
resultsAll four chemicals induced thymic atrophy and changes in both the relative proportion and absolute number of CD3(+), CD4(+)/CD8(-), CD4(-)/CD8(+), and CD4(+)/CD8(+) thymocytes. The most significant impact of exposure to DEX, DES, and CPS was modulation of gene expression in the T-cell receptor (TCR) complex and TCR and CD28 signaling pathways; this could represent a common mechanism of action and play a pivotal role in lineage commitment and development of T cells. Up-regulation of genes associated with the antigen presentation and dendritic cell maturation pathways was the most distinctive effect of TCDD exposure. These elements, which were also up-regulated by DEX and DES, contribute to positive and negative selection.
conclusionsGenomic analysis revealed gene expression changes in several pathways that are commonly associated with xenobiotic-induced immune system perturbations, particularly those that contribute to the development and maturation of thymic T cells.
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