Progress has been made in the study of natural immunomodulation mechanisms by acetylation modification.

Natural immune response is the body's first line of defense against pathogenic microbial invasion, playing a key role in killing pathogenic microorganisms, removing infected cells and maintaining a steady state in the body.
protein post-translational modifications (PTMs) are widely involved in regulating the activation of signal molecules in various paths.
non-histone acetytylation is important for regulating protein stability, enzyme activity, subcellular positioning, and protein-to-protein/DNA interactions.
years, the function of non-histoprotein acetylation modification in natural immune response has also been paid more and more attention.
but the regulation of signal molecular activity in natural immune responses by acetylation in collaboration with other post-translation modifications still needs to be explored.
Recently, the Wuhan Institute of Virology of the Chinese Academy of Sciences, the National Key Laboratory of Virology, the Center for Biosecurity Research Chen Jizheng, Chen Xinwen team found that HDAC3 in the body and outside the level can be positive natural immune response, acting on the signaling path in TBK1, and promote the production of type I interferon.
the study first found that TBK1 in the phase of viral infection is accompanied by the dynamic regulation of modified acetylation after translation, showing a trend of first strengthening and then weakening.
HDAC3 can directly deacetylize TBK1 Lys241, Lys692 bits to enhance TBK1 kinase activity, wherein TBK1 Lys241 bits of acetylation modification levels in the early stimulation of the virus significantly enhanced, followed by natural immune signaling pathacts to reduce.
further mechanism studies have found that acetylation at TBK1 Lys241-bits enhances the interaction between TBK1 and IRF3, while deacetylization at Lys241-bit enhances TBK1 phosphate IRF3.
study also found that the level of acetylation modification of TBK1 Lys692 bits also showed a trend of first strengthening and then weakening, and TBK1 Lys692 bit acetylation modification inhibited the activity of TBK1 diimosomes and their own kinase activity.
HDAC3 enhances TBK1 kinase activity by deacetylized TBK1, and TBK1 as a kinase can also enhance its deacetylase activity by phosphate HDAC3 Ser424 bits.
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