Research ArticleSKIN INFLAMMATION

Cutaneous innate immune tolerance is mediated by epigenetic control of MAP2K3 by HDAC8/9

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Science Immunology  21 May 2021:
Vol. 6, Issue 59, eabe1935
DOI: 10.1126/sciimmunol.abe1935

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Cutaneous chaos control by HDACs

The skin’s epidermal surface is routinely exposed to a diverse mix of physical, chemical, and microbial stimuli with proinflammatory potential. Epidermal keratinocytes have an innate tendency to tolerate this maelstrom by relying on the histone deacetylases HDAC8 and HDAC9 to restrain signaling pathways that can amplify local inflammation. Sawada et al. used transcriptomic profiling of human keratinocytes activated by poly I:C, a dsRNA mimic, to identify the kinase MAP2K3 as a pivotal target for regulation by HDAC8/9. Inhibition or silencing of HDAC8 or HDAC9 increased expression of MAP2K3 and activation of its downstream target p38MAPK. These findings provide a deeper understanding of how skin inflammation is normally held in check and pinpoint two kinases as potential targets for therapeutic inhibition in inflammatory skin diseases.

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