ArticleAutoimmune diseases2014
Differential immunotoxicity induced by two different windows of developmental trichloroethylene exposure.
Article in Autoimmune diseases, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 8 papers.
What it found
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Who cites it
8 citing papers in PubMed.
- Childhood cancer risk in offspring of mothers occupationally exposed to hydrocarbon solvents.European journal of cancer prevention : the official journal of the European Cancer Prevention Organisation (ECP) · 2026Article
- Irreversible effects of trichloroethylene on the gut microbial community and gut-associated immune responses in autoimmune-prone mice.Journal of applied toxicology : JAT · 2019Article
- Epigenetic underpinnings of developmental immunotoxicity and autoimmune disease.Current opinion in toxicology · 2018Article
- A single dose of trichloroethylene given during development does not substantially alter markers of neuroinflammation in brains of adult mice.Journal of immunotoxicology · 2017Article
- Inflammatory and oxidative stress-related effects associated with neurotoxicity are maintained after exclusively prenatal trichloroethylene exposure.Neurotoxicology · 2017Article
- Target Organ Metabolism, Toxicity, and Mechanisms of Trichloroethylene and Perchloroethylene: Key Similarities, Differences, and Data Gaps.The Journal of pharmacology and experimental therapeutics · 2016Review
- Epigenetic Toxicity of Trichloroethylene: A Single-Molecule Perspective.Toxicology research · 2016Article
- Developmental Activation of the AHR Increases Effector CD4+ T Cells and Exacerbates Symptoms in Autoimmune Disease-Prone Gnaq+/- Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2015Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
Developmental exposure to environmental toxicants may induce immune system alterations that contribute to adult stage autoimmune disease. We have shown that continuous exposure of MRL+/+ mice to trichloroethylene (TCE) from gestational day (GD) 0 to postnatal day (PND) 49 alters several aspects of CD4(+) T cell function. This window of exposure corresponds to conception-adolescence/young adulthood in humans. More narrowly defining the window of TCE developmental exposure causes immunotoxicity that would establish the stage at which avoidance and/or intervention would be most effective. The current study divided continuous TCE exposure into two separate windows, namely, gestation only (GD0 to birth (PND0)) and early-life only (PND0-PND49). The mice were examined for specific alterations in CD4(+) T cell function at PND49. One potentially long-lasting effect of developmental exposure, alterations in retrotransposon expression indicative of epigenetic alterations, was found in peripheral CD4(+) T cells from both sets of developmentally exposed mice. Interestingly, certain other effects, such as alterations in thymus cellularity, were only found in mice exposed to TCE during gestation. In contrast, expansion of memory/activation cell subset of peripheral CD4(+) T cells were only found in mice exposed to TCE during early life. Different windows of developmental TCE exposure can have different functional consequences.
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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.