Journal
AUTOPHAGY
Volume 19, Issue 6, Pages 1617-1618Publisher
TAYLOR & FRANCIS INC
DOI: 10.1080/15548627.2023.2187609
Keywords
Autophagy; inflammation; skin disease; tumor necrosis factor; ULK1 kinase complex
Categories
Ask authors/readers for more resources
TNF is an important cytokine that regulates immune responses to microbial infection. It can induce activation of NFKB/NF-kappa B or cell death through the formation of TNFRSF1A/TNFR1 complexes. Abnormal TNF-induced cell death is associated with human inflammatory diseases, and protective cell death checkpoints are crucial in preventing TNF cytotoxicity.
TNF (tumor necrosis factor) is an important cytokine that regulates immune responses in response to microbial infection. Two fates can be induced by TNF sensing, including activation of NFKB/NF-kappa B and cell death, which are mainly regulated by the formation of TNFRSF1A/TNFR1 (TNF receptor superfamily member 1A) complex I and complex II, respectively. Abnormal TNF-induced cell death leads to detrimental outcomes, underlying several human inflammatory diseases. The actions of protective brakes, or so-called specific cell death checkpoints, are important to prevent TNF cytotoxicity. A recent study published in Science characterizes novel functions of ATG9A, RB1CC1/FIP200 and TAX1BP1 as components of a previously undiscovered TNF-induced cell death checkpoint, independent of its roles in canonical macroautophagy/autophagy. Notably, this ATG9A-controlled cell-death checkpoint contributes to the prevention of inflammatory skin disease, demonstrating its crucial role in serving as a safeguard against the threat of TNF cytotoxicity.
Authors
I am an author on this paper
Click your name to claim this paper and add it to your profile.
Reviews
Recommended
No Data Available