Asset Details
Do you wish to reserve the book?
Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium
Hey, we have placed the reservation for you!
By the way, why not check out events that you can attend while you pick your title.
Oops! Something went wrong.
Looks like we were not able to place the reservation. Kindly try again later.
Are you sure you want to remove the book from the shelf?
Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium
Do you wish to request the book?
Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium
Please be aware that the book you have requested cannot be checked out. If you would like to checkout this book, you can reserve another copy
We have requested the book for you!
Your request is successful and it will be processed during the Library working hours. Please check the status of your request in My Requests.
Oops! Something went wrong.
Looks like we were not able to place your request. Kindly try again later.
Journal Article
Type I interferon induces necroptosis in macrophages during infection with Salmonella enterica serovar Typhimurium
2012
Overview
Salmonella enterica serovar Typhimurium (S. Typhimurium) is a virulent pathogen that induces rapid host death. Here we observed that host survival after infection with S. Typhimurium was enhanced in the absence of type I interferon signaling, with improved survival of mice deficient in the receptor for type I interferons (Ifnar1−/− mice) that was attributed to macrophages. Although there was no impairment in cytokine expression or inflammasome activation in Ifnar1−/− macrophages, they were highly resistant to S. Typhimurium–induced cell death. Specific inhibition of the kinase RIP1 or knockdown of the gene encoding the kinase RIP3 prevented the death of wild-type macrophages, which indicated that necroptosis was a mechanism of cell death. Finally, RIP3-deficient macrophages, which cannot undergo necroptosis, had similarly less death and enhanced control of S. Typhimurium in vivo. Thus, we propose that S. Typhimurium induces the production of type I interferon, which drives necroptosis of macrophages and allows them to evade the immune response.
Publisher
Nature Publishing Group US,Nature Publishing Group
Subject
/ Animals
/ Biomedical and Life Sciences
/ GTPase-Activating Proteins - antagonists & inhibitors
/ GTPase-Activating Proteins - metabolism
/ Interferon Type I - immunology
/ Interferon Type I - metabolism
/ Mice
/ Receptor, Interferon alpha-beta - deficiency
/ Receptor, Interferon alpha-beta - genetics
/ Receptor-Interacting Protein Serine-Threonine Kinases - antagonists & inhibitors
/ Receptor-Interacting Protein Serine-Threonine Kinases - deficiency
/ Receptor-Interacting Protein Serine-Threonine Kinases - genetics
/ Salmonella Infections, Animal - immunology
/ Salmonella Infections, Animal - metabolism
/ Salmonella Infections, Animal - microbiology
/ Salmonella typhimurium - immunology
/ Salmonella typhimurium - pathogenicity
/ Survival
