ArticleToxicological sciences : an official journal of the Society of Toxicology2015
Developmental Activation of the AHR Increases Effector CD4+ T Cells and Exacerbates Symptoms in Autoimmune Disease-Prone Gnaq+/- Mice.
Article in Toxicological sciences : an official journal of the Society of Toxicology, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 17 papers.
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Who cites it
17 citing papers in PubMed, 20 citations in OpenAlex.
- Article
- Expanded assessment of xenobiotic associations with antinuclear antibodies in the United States, 1988-2012.Environment international · 2022Article
- DNA Methylation Patterns inEnvironmental health perspectives · 2021Article
- Dioxin Disrupts Dynamic DNA Methylation Patterns in Genes That Govern Cardiomyocyte Maturation.Toxicological sciences : an official journal of the Society of Toxicology · 2020Article
- Developmental 2,3,7,8-tetrachlorodibenzo-p-dioxin exposure of either parent enhances the risk of necrotizing enterocolitis in neonatal mice.Birth defects research · 2020Article
- The Ancestral Environment Shapes Antiviral CD8iScience · 2019Article
- Early life exposures shape the CD4Scientific reports · 2019Article
- Epigenetic underpinnings of developmental immunotoxicity and autoimmune disease.Current opinion in toxicology · 2018Article
- Developmental Exposure to a Mixture of 23 Chemicals Associated With Unconventional Oil and Gas Operations Alters the Immune System of Mice.Toxicological sciences : an official journal of the Society of Toxicology · 2018Article
- Sex-Dependent Influence of Developmental Toxicant Exposure on Group B Streptococcus-Mediated Preterm Birth in a Murine Model.Reproductive sciences (Thousand Oaks, Calif.) · 2018Article
- Aryl hydrocarbon receptor signaling modulates antiviral immune responses: ligand metabolism rather than chemical source is the stronger predictor of outcome.Scientific reports · 2018Article
- The Aryl Hydrocarbon Receptor as an Immune-Modulator of Atmospheric Particulate Matter-Mediated Autoimmunity.Frontiers in immunology · 2018Review
- Environmental cues received during development shape dendritic cell responses later in life.PloS one · 2018Article
- Does the Aryl Hydrocarbon Receptor Regulate Pluripotency?Current opinion in toxicology · 2017Article
- GMediators of inflammation · 2017Article
- Immunomodulation By Subchronic Low Dose 2,3,7,8-Tetrachlorodibenzo-p-Dioxin in Experimental Autoimmune Encephalomyelitis in the Absence of Pertussis Toxin.Toxicological sciences : an official journal of the Society of Toxicology · 2016Article
- Environmental Immunology: Lessons Learned from Exposure to a Select Panel of Immunotoxicants.Journal of immunology (Baltimore, Md. : 1950) · 2016Review
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Authors and funding
6 authors at 1 institution in 1 country.
Funding
Abstract
Perinatal environmental exposures are potentially important contributors to the increase in autoimmune diseases. Yet, the mechanisms by which these exposures increase self-reactive immune responses later in life are poorly understood. Autoimmune diseases require CD4(+) T cells for initiation, progression, and/or clinical symptoms; thus, developmental exposures that cause durable changes in CD4(+) T cells may play a role. Early life activation of the aryl hydrocarbon receptor (AHR) causes persistent changes in the response of CD4(+) T cells to infection later in life but whether CD4(+) T cells are affected by developmental exposure in the context of an autoimmune disease is unknown. Gnaq(+/-) mice develop symptoms of autoimmune disease similar to those measured clinically, and therefore can be used to evaluate gene-environment interactions during development on disease progression. Herein, we examined the effect of AHR activation in utero and via lactation, or solely via lactation, on disease onset and severity in adult Gnaq(+/-) offspring. Developmental activation of the AHR-accelerated disease in Gnaq(+/-) mice, and this correlates with increases in effector CD4(+) T-cell populations. Increased symptom onset and cellular changes due to early life AHR activation were more evident in female Gnaq(+/-) mice compared with males. These observations suggest that developmental AHR activation by pollutants, and other exogenous ligands, may increase the likelihood that genetically predisposed individuals will develop clinical symptoms of autoimmune disease later in life.
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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.