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Updated: Jan 30, 2026
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Author Spotlight: Self-Assessment Protocol for Predicting Psoriatic Arthritis in Psoriasis Patients
Published on: March 1, 2024
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Psoriasis and the TNF/IL23/IL17 axis.
Kazuhisa Furue1, Takamichi Ito1, Gaku Tsuji1
1Department of Dermatology, Graduate School of Medical Sciences, Kyushu University, Fukuoka, Japan.
Summary
Psoriasis treatment with biologics targeting the tumor necrosis factor (TNF)/interleukin (IL) 23/IL-17 axis highlights its central role. Keratinocytes and immune cells create a feedback loop, with anti-IL-23/IL-17 therapies showing promise for skin lesions.
Area of Science:
- Immunodermatology
- Molecular biology of skin inflammation
Background:
- The tumor necrosis factor (TNF)/interleukin (IL) 23/IL-17 axis is critical in psoriasis pathogenesis.
- Both immune cells and non-hematopoietic keratinocytes contribute to this axis through cytokine production.
Purpose of the Study:
- To review recent advancements concerning psoriasis and the TNF/IL23/IL17 axis.
- To highlight the interplay between immune cells and keratinocytes in psoriasis.
Main Methods:
- Literature review of current research on psoriasis and the TNF/IL23/IL17 axis.
- Analysis of the role of specific cytokines (TNF, IL-23, IL-17A, IL-17C) in disease development.
Main Results:
- The TNF/IL23/IL17 axis is crucial for psoriasis development, involving both immune cells and keratinocytes.
- Crosstalk between these cell types forms a feed-forward loop amplifying the axis.
- Anti-IL-23/IL-17 biologics may be more effective than anti-TNF-α therapies for skin lesions in psoriatic arthritis.
Conclusions:
- The TNF/IL23/IL17 axis is a key therapeutic target in psoriasis.
- Understanding keratinocyte and immune cell crosstalk is vital for developing targeted therapies.
- Emerging biologics targeting IL-23 and IL-17 show significant potential for managing psoriasis skin manifestations.
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