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Fig. 2 | Particle and Fibre Toxicology

Fig. 2

From: Human exposure to diesel exhaust induces CYP1A1 expression and AhR activation without a coordinated antioxidant response

Fig. 2

Schematic presentation of AhR activation and co-localization of leukocyte nuclear AhR with CD3 cells. Panel A Schematic presentation of AhR activation and interaction with other molecules regulating the induction of genes encoding pro- and anti-inflammatory responses [28, 29]. In the inactive state AhR is found in the cytoplasm associated with protein complexes such as Hsp90 and Src. Following activation, AhR is released from these complexes. The conformationally changed AhR, translocate to the nucleus and dimerizes with Aryl hydrocarbon receptor nuclear translocator (ARNT) factor to target genes such as CYP1A1 and AhRR (aryl hydrocarbon receptor repressor), or to interact with other transcription factors. In addition, the released associated proteins such as Src, may interact with epidermal growth factor receptor (EGFR) and cause MAPKs signalling cascades (Black arrows). The green frame illustrates pathways by which activated AhR, targets genes (genomic pathway) and/or interact with other regulatory molecules (Non genomic pathway) to control these responses in the epithelium. The red frame illustrates AhR within bronchial submucosal leukocytes that may be activated in different cells and involved in the regulation of the immune response. Panel B Immunoreactivity within the bronchial submucosa to CD3 antibody (upper left) and corresponding biopsy section stained for AhR antibody (upper right), following DE exposure. Scale bars = 100 μm (micro meters). Lower panel (in panel B) images are enlargements of red frames from upper panel (in panel B) and show co-localization of CD3+ lymphocytes and leukocytes AhR nuclear translocation (bold arrows), narrow arrows show nuclear AhR in leukocytes, Scale bars = 50 μm (micro meters)

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