期刊
FASEB JOURNAL
卷 34, 期 10, 页码 13156-13170出版社
WILEY
DOI: 10.1096/fj.202001607R
关键词
AIM2; autoimmune disease; cGAMP; DAMP; pulmonary disease
资金
- David and Christine Cugell Fellowship
- Gorter Family Foundation
- Stanley Manne Children's Research Institute
- Ann & Robert H. Lurie Children's Hosptial of Chicago
- NIH [P01HL071643, R01HL128194, P01AG049665]
The presence of DNA in the cytosol is usually a sign of microbial infections, which alerts the host innate immune system to mount a defense response. Cyclic GMP-AMP synthase (cGAS) is a critical cytosolic DNA sensor that elicits robust innate immune responses through the production of the second messenger, cyclic GMP-AMP (cGAMP), which binds and activates stimulator of interferon genes (STING). However, cGAS binds to DNA irrespective of DNA sequence, therefore, self-DNA leaked from the nucleus or mitochondria can also serve as a cGAS ligand to activate this pathway and trigger extensive inflammatory responses. Dysregulation of the cGAS-STING pathway is responsible for a broad array of inflammatory and autoimmune diseases. Recently, evidence has shown that self-DNA release and cGAS-STING pathway over-activation can drive lung disease, making this pathway a promising therapeutic target for inflammatory lung disease. Here, we review recent advances on the cGAS-STING pathway governing self-DNA sensing, highlighting its role in pulmonary disease.
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