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Updated: Oct 29, 2025
10:42
Generation and Culturing of Primary Human Keratinocytes from Adult Skin
Published on: December 22, 2017
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Keratin 17 in psoriasis: Current understanding and future perspectives.
Yiting Lin1, Weigang Zhang1, Bing Li1
1Department of Dermatology, Xijing Hospital, Fourth Military Medical University, Xi'an, Shaanxi, China.
Seminars in Cell & Developmental Biology
|July 7, 2021
Summary
Keratin 17 (K17) is overexpressed in psoriasis, promoting keratinocyte proliferation and inflammation. A K17/T-cell/cytokine loop drives this autoimmune skin disease, with K17-targeted therapies showing promise.
Area of Science:
- Dermatology
- Immunology
- Cell Biology
Background:
- Keratin 17 (K17) is a cytoskeletal protein typically absent in normal epidermis.
- K17 is significantly overexpressed in the suprabasal layer of the epidermis in psoriasis.
Purpose of the Study:
- To review the pathogenic roles of K17 in psoriasis.
- To elucidate the mechanisms behind K17 overexpression in psoriasis.
- To discuss the therapeutic potential of targeting K17.
Main Methods:
- Review of existing literature on K17 function and expression in psoriasis.
- Analysis of K17's pro-proliferative and pro-inflammatory effects on keratinocytes.
- Investigation of K17 peptide-mediated T-cell activation and cytokine production.
Main Results:
- K17 promotes keratinocyte proliferation and inflammation.
- K17 peptides activate autoreactive T cells, leading to psoriasis-related cytokine release.
- Cytokines modulate K17 expression and function, forming a pathogenic autoimmune loop.
Conclusions:
- A K17/T-cell/cytokine autoimmune loop is central to psoriasis pathogenesis.
- Targeting K17 demonstrates therapeutic potential in preclinical psoriasis models.
- Further research into K17 pathways may reveal new treatment strategies for psoriasis.
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