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DLX3-Dependent STAT3 Signaling in Keratinocytes Regulates Skin Immune Homeostasis
Shreya Bhattacharya1, Jin-Chul Kim1, Youichi Ogawa2
1Laboratory of Skin Biology, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institutes of Health, Bethesda, Maryland, USA.
The Journal of Investigative Dermatology
|December 17, 2017
Summary
Deleting DLX3 in skin cells triggers inflammation and a psoriasis-like condition by activating STAT3 signaling. This highlights DLX3
Area of Science:
- Dermatology
- Molecular Biology
- Immunology
Background:
- Dermal inflammation and keratinocyte differentiation are complex processes.
- The transcription factor DLX3 plays a role in skin homeostasis.
- Dysregulation of DLX3 is linked to inflammatory skin conditions.
Purpose of the Study:
- To investigate the role of DLX3 in epidermal homeostasis.
- To identify the molecular signals initiated by DLX3-deficient keratinocytes.
- To explore the therapeutic potential of targeting STAT3 signaling in DLX3-related skin inflammation.
Main Methods:
- Tamoxifen-inducible epidermal deletion of DLX3 in mice (Krt14-cre/ERT;DLX3fl/fl).
- Gene expression analysis (RNA-seq) and cytokine profiling.
- Pharmacological inhibition of STAT3 activation.
Main Results:
- DLX3 ablation led to disrupted keratinocyte differentiation and increased pro-inflammatory cytokines (IL-17, IL-36).
- Accumulation of immune cells (Langerhans cells, macrophages, γδ T cells) observed.
- Activated STAT3 identified as a key regulator; STAT3 inhibition attenuated the inflammatory phenotype.
Conclusions:
- DLX3 is crucial for maintaining skin homeostasis by regulating the STAT3 signaling network.
- STAT3 activation is a critical downstream event in DLX3-deficient keratinocytes.
- Targeting STAT3 may offer a therapeutic strategy for DLX3-associated inflammatory skin diseases.
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