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Publication Detail

Title: Early life exposures shape the CD4+ T cell transcriptome, influencing proliferation, differentiation, and mitochondrial dynamics later in life.

Authors: Burke, Catherine G; Myers, Jason R; Boule, Lisbeth A; Post, Christina M; Brookes, Paul S; Lawrence, B Paige

Published In Sci Rep, (2019 08 07)

Abstract: Early life environmental exposures drive lasting changes to the function of the immune system and can contribute to disease later in life. One of the ways environmental factors act is through cellular receptors. The aryl hydrocarbon receptor (AHR) is expressed by immune cells and binds numerous xenobiotics. Early life exposure to chemicals that bind the AHR impairs CD4+ T cell responses to influenza A virus (IAV) infection in adulthood. However, the cellular mechanisms that underlie these durable changes remain poorly defined. Transcriptomic profiling of sorted CD4+ T cells identified changes in genes involved in proliferation, differentiation, and metabolic pathways were associated with triggering AHR during development. Functional bioassays confirmed that CD4+ T cells from infected developmentally exposed offspring exhibit reduced proliferation, differentiation, and cellular metabolism. Thus, developmental AHR activation shapes T cell responsive capacity later in life by affecting integrated cellular pathways, which collectively alter responses later in life. Given that coordinated shifts in T cell metabolism are essential for T cell responses to numerous challenges, and that humans are constantly exposed to many different types of AHR ligands, this has far-reaching implications for how AHR signaling, particularly during development, durably influences T cell mediated immune responses across the lifespan.

PubMed ID: 31391494 Exiting the NIEHS site

MeSH Terms: Adult; Animals; Basic Helix-Loop-Helix Transcription Factors/metabolism*; CD4-Positive T-Lymphocytes/immunology*; CD4-Positive T-Lymphocytes/metabolism; Cell Differentiation/immunology; Cell Proliferation; Child; Child Development; Disease Models, Animal; Environmental Pollutants/immunology*; Female; Humans; Influenza A virus/immunology; Influenza, Human/blood; Influenza, Human/immunology*; Influenza, Human/virology; Ligands; Male; Mice; Mitochondrial Dynamics/immunology; RNA-Seq; Receptors, Aryl Hydrocarbon/metabolism*; Transcriptome/immunology*

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