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Updated: Aug 6, 2026
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High-throughput Quantitative Real-time RT-PCR Assay for Determining Expression Profiles of Types I and III Interferon Subtypes
Published on: March 24, 2015
Keratin 16 puts the brakes on type I interferon signalling
Syed F H Shah1, Catherine Y Liao2, Edel A O'Toole1
1Centre for Cell Biology and Cutaneous Research, Blizard Institute, Queen Mary University of London, London, UK; Department of Dermatology, Royal London Hospital, Barts Health NHS Trust, London, UK.
Trends in Molecular Medicine
|July 20, 2026
Summary
Stress-induced keratin 16 (KRT16) regulates skin immunity by suppressing type I interferon signaling. Loss of KRT16 in pachyonychia congenita amplifies this inflammatory pathway, suggesting KRT16 as a therapeutic target.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Keratin 16 (KRT16) is a keratin protein involved in skin structure.
- Innate immunity relies on signaling pathways to detect and respond to pathogens.
- Type I interferons (IFNs) are crucial cytokines in antiviral and immune responses.
Purpose of the Study:
- To investigate the role of keratin 16 (KRT16) in regulating skin innate immunity.
- To elucidate the mechanism by which KRT16 influences type I interferon signaling.
- To explore the therapeutic potential of targeting the KRT16-IFN axis.
Main Methods:
- Studied stress-induced expression of KRT16 in skin.
- Investigated KRT16's interaction with 14-3-3ε protein.
- Analyzed the impact of KRT16 on retinoic acid-inducible gene I (RIG-I)-mediated IFN signaling.
- Examined KRT16 function in a mouse model of pachyonychia congenita.
Main Results:
- Stress-induced KRT16 acts as a regulator of skin innate immunity.
- KRT16 suppresses type I IFN signaling by sequestering 14-3-3ε, thereby inhibiting RIG-I.
- Loss of KRT16 leads to amplified inflammatory IFN signaling, observed in pachyonychia congenita.
Conclusions:
- The KRT16-IFN signaling axis is a key component of skin immune regulation.
- KRT16 plays a suppressive role in the inflammatory response mediated by type I IFNs.
- Targeting the KRT16-IFN pathway presents a potential therapeutic strategy for inflammatory skin conditions.
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