Loss of Nrf2 in bone marrow-derived macrophages impairs antigen-driven CD8+ T cell function by limiting GSH and Cys availability

Author:

Sha Lisa K.,Sha Weixiao,Kuchler Laura,Daiber Andreas,Giegerich Annika K.,Weigert Andreas,Knape Tilo,Snodgrass Ryan,Schröder Katrin,Brandes Ralf P.,Brüne Bernhard,von Knethen Andreas

Funder

Else Kröner-Fresenius Foundation (EKFS)

Research Training Group Translational Research Innovation - Pharma (TRIP)

Deutsche Forschungsgemeinschaft

Publisher

Elsevier BV

Subject

Physiology (medical),Biochemistry

Reference51 articles.

1. Nrf2–Keap1 defines a physiologically important stress response mechanism;Motohashi;Trends Mol. Med.,2004

2. Antioxidants and phase 2 enzymes in macrophages: regulation by Nrf2 signaling and protection against oxidative and electrophilic stress;Zhu;Exp. Biol. Med. (Maywood),2008

3. Transcription factor Nrf2 regulates inflammation by mediating the effect of 15-deoxy-Delta(12,14)-prostaglandin j(2);Itoh;Mol. Cell.. Biol.,2004

4. Nrf2-dependent protection from LPS induced inflammatory response and mortality by CDDO-imidazolide;Thimmulappa;Biochem. Biophys. Res. Commun.,2006

5. Macrophage-derived nitric oxide regulates T cell activation via reversible disruption of the Jak3/STAT5 signaling pathway;Bingisser;J. Immunol.,1998

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