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Murine Model of Epicutaneously-Induced Immunomodulation
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Reprogramming immunity at the metabolic-epidermal interface in obesity-associated psoriasis
Jinsun Jang1, Minji Park1, Hee Joo Kim2
1Department of Health Science and Technology, Gachon Advanced Institute for Health Science & Technology, Gachon University, Incheon 21999, Republic of Korea.
Cytokine & Growth Factor Reviews
|January 14, 2026
Summary
Obesity worsens psoriasis by causing metabolic stress that fuels inflammation and reduces treatment effectiveness. Restoring metabolic health can improve immune responses and sustain remission in this chronic inflammatory skin condition.
Area of Science:
- Integrative immunology and metabolic disease research.
- Dermatology and chronic inflammatory disorders.
Background:
- Obesity and psoriasis are linked chronic inflammatory conditions.
- Metabolic overload in obesity drives immune dysfunction and treatment resistance in psoriasis.
Purpose of the Study:
- To review the mechanistic and clinical links between obesity and psoriasis.
- To discuss strategies for restoring metabolic-immune balance for disease management.
Main Methods:
- Integration of mechanistic insights from multi-omics, single-cell, and spatial studies.
- Clinical data analysis on body mass index, insulin resistance, and therapeutic responses.
- Review of metabolic interventions and their impact on immune responses.
Main Results:
- Obesity transforms adipose tissue into an inflammatory organ, reprogramming skin cells and immune cells.
- Metabolic stress, including impaired mitochondrial function and epigenetic changes, perpetuates inflammation.
- Increased body mass index and insulin resistance correlate with poor response to biologic therapies (TNF, IL-17, IL-23).
Conclusions:
- Obesity-associated psoriasis is an inflammatory state imprinted by chronic metabolic stress.
- Metabolic interventions can enhance responsiveness to psoriasis treatments.
- Restoring metabolic-immune plasticity is key for sustained remission.
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