Mitochondrial DNA damage caused by antiviral innate immune response

Recently, researchers from leading international online journal nature, Yale University School of Medicine, published their results of a new study, they found that the antiviral innate immune process, mitochondria play a crucial role.

Under normal conditions, the mitochondrial DNA (mtDNA) within each cell there are thousands of copies, and is packaged into hundreds of higher-order structure, called the nucleoid. TFAM binding protein is responsible for a large number of mtDNA class nuclear regulatory structure, as well as the number of mutual isolation. Completely remove the mtDNA would seriously damage the process of oxidative phosphorylation, calcium-dependent trigger stress signaling and metabolic adaptive responses. However, observed in a number of human diseases and the aging process the cells are still not well defined on the response mtDNA instability. Researchers proved by TFAM defects caused due to stress will moderate mtDNA antiviral signaling pathways involved in cell and enhance a series of interferon-stimulated gene expression. In the mechanism, they found Rabbit C-Peptide ELISA Kit http://www.cusabio.com/ELISA_Kit-115364/ will promote mtDNA escape into the cytoplasm, is captured DNA receptors cGAS, promote STING-IRF3-dependent signaling pathways, leading to increase in interferon-stimulated gene expression, enhanced type I interferon response, and promote cell resist the effects of the virus. In addition, the spore measles virus can induce mtDNA stress, enhanced signaling pathways stage of infection and type I interferon antiviral response.

In summary, results of this study showed that the immune response is critical for mitochondrial natural, mtDNA intrinsic stress is a cell antiviral signaling switch, suggesting that cells may by monitored mtDNA balance, coordination classic viral induction of innate immune mechanisms started anti-virus system.