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Dendritic cells death induced by contact sensitizers is controlled by Nrf2 and depends on glutathione levels.pdfVIP

Dendritic cells death induced by contact sensitizers is controlled by Nrf2 and depends on glutathione levels.pdf

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Dendritic cells death induced by contact sensitizers is controlled by Nrf2 and depends on glutathione levels.pdf

Toxicology and Applied Pharmacology 322 (2017) 41–50 Contents lists available at ScienceDirect Toxicology and Applied Pharmacology journal homepage: /locate/taap Dendritic cells death induced by contact sensitizers is controlled by Nrf2 and depends on glutathione levels☆ Zeina El Ali a, Claudine Deloménie b, Jérémie Botton c, Marc Pallardy a, Saadia Kerdine-R?mer a,? a UMR996 - In?ammation, Chemokines and Immunopathology-, INSERM, Univ Paris-Sud, Université Paris-Saclay, 92296 Chatenay-Malabry, France b IFR141 IPSIT, Univ Paris-Sud, Université Paris-Saclay, Chatenay-Malabry, France c INSERM, UMR1153 Epidemiology and Biostatistics Sorbonne Paris Cité Center (CRESS), Team article info Article history: Received 25 June 2016 Revised 31 January 2017 Accepted 16 February 2017 Available online 20 February 2017 Keywords: Allergy Dendritic cells Nrf2 Contact sensitizers Reactive species GSH, Apoptosis bcl-2 ho-1 abstract Dendritic cells (DC) are known to play a major role during contact allergy induced by contact sensitizers (CS). Our previous studies showed that Nrf2 was induced in DC and controlled allergic skin in?ammation in mice in response to chemicals. In this work, we raised the question of the role of Nrf2 in response to a stress provoked by chemical sensitizers in DC. We used two well-described chemical sensitizers, dinitrochlorobenzene (DNCB) and cinnamaldehyde (CinA), known to have different chemical reactivity and mechanism of action. First, we performed a RT-qPCR array showing that CinA was a higher inducer of immune and detoxi?cation genes compared to DNCB. Interestingly, in the absence of Nrf2, gene expression was dramatically affected in response to DNCB but was slightly affected in response to CinA. These observations prompted us to study DCs cell death in response to both chemicals. DNCB and CinA increased apoptotic cells and decreased living cells in the absence of Nrf2. The characterization of DC apoptosis induced by both CS involved the mitochondrial-de

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