Regular ArticleDistribution and Behavior of the Ah Receptor in Murine T Lymphocytes
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Cited by (46)
Immunotoxicology of Halogenated Aromatic Hydrocarbons
2018, Comprehensive Toxicology: Third EditionCross-talk between aryl hydrocarbon receptor and the inflammatory response: A role for nuclear factor-κB
2014, Journal of Biological ChemistryCitation Excerpt :Immunohistochemical analysis of embryonic tissues showed that AhR expression is developmentally regulated (13). Stimulation of resting T cells with mitogens resulted in a marked increase of AhR expression (14, 15), whereas TGF-β inhibits or increases the expression of AhR and genes of the AhR gene battery in a cell-specific manner (16, 17). In this study, we elucidated the molecular mechanisms responsible for regulating AhR expression during inflammatory responses.
Potential protective mechanisms of aryl hydrocarbon receptor (AHR) signaling in benign prostatic hyperplasia
2011, DifferentiationCitation Excerpt :A prominent physiological response of AHR activation is suppression of innate and humoral immunity. The AHR is expressed in a diverse spectrum of immune cells including macrophages, cytotoxic and regulatory T cells, dendritic cells, and neutrophils (Komura et al., 2001; Vorderstrasse and Kerkvliet, 2001; Ackermann et al., 1989; Lawrence et al., 1996). TCDD-induced AHR activation has been shown to suppress inflammatory cytokine production by macrophages stimulated with lipopolysaccharide (Kimura et al., 2009), and inhibit polymorphonucleocyte cytolytic and cytostatic activity (Ackermann et al., 1989).
Microarray analysis of the AHR system: Tissue-specific flexibility in signal and target genes
2007, Toxicology and Applied PharmacologyA constitutively active arylhydrocarbon receptor induces growth inhibition of jurkat T cells through changes in the expression of genes related to apoptosis and cell cycle arrest
2004, Journal of Biological ChemistryCitation Excerpt :Our recent finding that primary T cells have functional AhR also supports this mechanism (19). In the present study, to investigate the effects of activated AhR on T cells and their underlying mechanism, we transiently expressed a constitutively active AhR (CA-AhR) mutant in human leukemic Jurkat T cells, because all the T cell lines examined thus far, including Jurkat T cells, do not have functional AhR (20, 21). We used a CA-AhR mutant lacking the minimal PAS B motif, which is constitutively localized in the nucleus and activates AhR-dependent transcription independent of the ligand (22, 23).
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