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Updated: May 4, 2026
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Purification of Human S100A12 and Its Ion-induced Oligomers for Immune Cell Stimulation
Published on: September 29, 2019
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S100A8-S100A9 protein complex mediates psoriasis by regulating the expression of complement factor C3
Helia B Schonthaler1, Juan Guinea-Viniegra1, Stefanie K Wculek1
1BBVA Foundation-CNIO Cancer Cell Biology Programme, Spanish National Cancer Research Centre (CNIO), 29029 Madrid, Spain.
Immunity
|December 17, 2013
Summary
Researchers identified S100A8-S100A9 (calprotectin) and complement component C3 as key proteins in psoriasis. Targeting these may offer new therapeutic strategies for this inflammatory skin disease.
Area of Science:
- Dermatology
- Immunology
- Molecular Biology
Background:
- Psoriasis is a prevalent inflammatory skin condition with complex causes and few treatments.
- Identifying novel molecular players is crucial for developing effective therapies.
Purpose of the Study:
- To investigate the proteomic landscape of psoriatic epidermis.
- To elucidate the role of upregulated proteins in psoriasis pathogenesis.
- To explore potential therapeutic targets for psoriasis.
Main Methods:
- Proteomic analysis of human psoriatic skin samples.
- In vitro studies using mouse and human cells to assess protein function.
- Genetic deletion of S100A9 in mouse models of skin inflammation.
- Pharmacological inhibition of complement component C3 in mouse models.
Main Results:
- S100A8-S100A9 (calprotectin) and complement component C3 were the most upregulated proteins in psoriatic epidermis.
- S100A9 binds to chromatin and modulates C3 gene expression.
- Genetic deletion of S100A9 significantly reduced psoriasis-like skin disease and inflammation in mice.
- Inhibition of C3 also markedly decreased the severity of skin inflammation in mouse models.
Conclusions:
- S100A8-S100A9 regulates C3 expression at the nuclear level.
- The S100A8-S100A9/C3 axis represents a promising therapeutic target for psoriasis treatment.
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