ArticleEnvironmental health perspectives2014
Effects of developmental activation of the AhR on CD4+ T-cell responses to influenza virus infection in adult mice.
Article in Environmental health perspectives, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 28 papers.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
28 citing papers in PubMed, 40 citations in OpenAlex.
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- Exposure to a mixture of 23 chemicals associated with unconventional oil and gas operations alters immune response to challenge in adult mice.Journal of immunotoxicology · 2021Article
- Developmental Origins of Delayed Adult Immune Response: The AhR Connection.Environmental health perspectives · 2021Article
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- 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
- 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
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- Environmental cues received during development shape dendritic cell responses later in life.PloS one · 2018Article
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3 authors at 1 institution in 1 country.
Funding
Abstract
backgroundEpidemiological and animal studies indicate that maternal exposure to pollutants that bind the aryl hydrocarbon receptor (AhR) correlates with poorer ability to combat respiratory infection and lower antibody levels in the offspring. These observations point to an impact on CD4+ T cells. Yet, the consequence of developmental exposure to AhR ligands on the activation and differentiation of CD4+ T cells has not been directly examined.
objectivesOur goal was to determine whether maternal exposure to an AhR ligand directly alters CD4+ T cell differentiation and function later in life.
methodsC57BL/6 mice were exposed to a prototypical AhR ligand, 2,3,7,8-tetrachlorodibenzo-p-dioxin (TCDD), in utero and via suckling. We then measured CD4+ T-cell activation and differentiation into distinct effector populations in adult offspring that were infected with influenza A virus (IAV). Reciprocal adoptive transfers were used to define whether modifications in CD4+ T-cell responses resulted from direct effects of developmental TCDD exposure on CD4+ T cells.
resultsDevelopmental exposure skewed CD4+ T-cell responses to IAV infection. We observed fewer virus-specific, activated CD4+ T cells and a reduced frequency of conventional CD4+ effector-cell subsets. However, there was an increase in regulatory CD4+ T cells. Direct effects of AhR activation on CD4+ T cells resulted in impaired differentiation into conventional effector subsets; this defect was transferred to mice that had not been developmentally exposed to TCDD.
conclusionsMaternal exposure to TCDD resulted in durable changes in the responsive capacity and differentiation of CD4+ T cells in adult C57BL/6 mice.
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