Related Experiment Video
Updated: Jan 14, 2026
10:42
Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
17.3K
CD271 orchestrates skin structure, differentiation, and inflammation via PI3K/Akt and PKCα/ERK pathways
Marika Quadri1, Luca Reggiani Bonetti2, Cristina Pellegrini3
1DermoLAB, Department of Surgical, Medical, Dental and Morphological Science, University of Modena and Reggio Emilia, Modena, Italy.
Cell Death & Disease
|October 21, 2025
Summary
CD271 is crucial for skin homeostasis. Its absence in mouse models causes epidermal hyperproliferation and inflammation, resembling skin diseases and offering new therapeutic avenues.
Area of Science:
- Dermatology and Molecular Biology
- Neurotrophin signaling in skin physiology
Background:
- The neurotrophin receptor CD271 is involved in pathological skin conditions like psoriasis and squamous cancer.
- CD271 mediates keratinocyte responses, influencing stem cell transitions, but in vivo models were lacking.
Purpose of the Study:
- To develop and characterize novel mouse models (CD271cKO and CD271ciKO) to study CD271's role in skin homeostasis in vivo.
- To investigate the effects of CD271 deletion on keratinocyte behavior and inflammatory responses.
Main Methods:
- Development of conditional knockout mouse models (CD271cKO, CD271ciKO) with CD271 deletion in keratinocytes.
- Histology, functional assays, transcriptomics, and molecular analyses were performed on knockout skin.
Main Results:
- CD271 deletion led to epidermal hyperproliferation, an "activated" keratinocyte signature, and delayed differentiation.
- Upregulation of proliferation markers (Ki67, PCNA), keratin genes (KRT5, KRT6), and inflammatory cytokines (IL1α, Cxcl15, TGFβ) was observed.
- KO skin exhibited immune cell recruitment (T cells, macrophages, neutrophils) and activation of inflammatory pathways (TNF, JAK/Stat, IL17, PI3k/Akt).
Conclusions:
- CD271 is a critical regulator of skin homeostasis.
- The developed mouse models are valuable tools for studying CD271-related skin pathophysiology and developing therapies.
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