[HTML][HTML] Nrf2 is a critical regulator of the innate immune response and survival during experimental sepsis

RK Thimmulappa, H Lee, T Rangasamy… - The Journal of …, 2016 - Am Soc Clin Investig
The Journal of clinical investigation, 2016Am Soc Clin Investig
Sepsis and sepsis syndrome are leading causes of mortality throughout the world. It is
widely held that sepsis represents a dysregulated innate immune response to an offending
pathogen. This immune response is often initiated via microbial products signaling through
TLRs expressed on host immune cells. There is increasing evidence that this innate
response can be dramatically influenced by the cellular redox state, and thus a better
understanding of oxidative regulation of innate immunity could lead to new treatments for …
Sepsis and sepsis syndrome are leading causes of mortality throughout the world. It is widely held that sepsis represents a dysregulated innate immune response to an offending pathogen. This immune response is often initiated via microbial products signaling through TLRs expressed on host immune cells. There is increasing evidence that this innate response can be dramatically influenced by the cellular redox state, and thus a better understanding of oxidative regulation of innate immunity could lead to new treatments for sepsis. In this issue of the JCI, Thimmulappa et al. show that nuclear factor-erythroid 2–related factor 2 (Nrf2), a member of the “cap’n’collar” family of basic region–leucine zipper transcription factors, which has previously been shown to be involved in the transcription of antioxidant gene expression in response to xenobiotic stress, is also a critical regulator of cellular oxidative stress in sepsis (see the related article beginning on page 984).
The Journal of Clinical Investigation