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KLF4 modulates macrophage-driven inflammation in diabetic psoriasis-like dermatitis through the TIMP3-ADAM17 axis: A

Meichen Jin1, Yiyao Li2, Yuan Kong2

  • 1Department of Dermatology, General Hospital of Northern Theater Command, No. 83, Wenhua Road, Shenhe District, Shenyang City, Liaoning Province 110000, China.

Clinical Immunology (Orlando, Fla.)
|July 31, 2026
PubMed

Insights

Krüppel-like factor 4 (KLF4) is downregulated in type 2 diabetes mellitus (T2DM) with psoriasis. KLF4 overexpression improved metabolic function and reduced skin inflammation in a diabetic psoriasis mouse model.

Area of Science:

  • Immunology
  • Dermatology
  • Metabolic Disorders

Background:

  • Type 2 diabetes mellitus (T2DM) and psoriasis often coexist, presenting complex inflammatory challenges.
  • Macrophage-mediated inflammation plays a critical role in the pathogenesis of both conditions.
  • Krüppel-like factor 4 (KLF4) is a transcription factor with known roles in immune regulation and metabolic processes.

Purpose of the Study:

  • To investigate the role of Krüppel-like factor 4 (KLF4) in macrophage-mediated inflammation in patients with T2DM and psoriasis.
  • To evaluate the therapeutic potential of KLF4 in a preclinical model of diabetic psoriasis-like dermatitis.

Main Methods:

  • Measurement of KLF4, TIMP3, and ADAM17 levels in skin samples from patients with T2DM and psoriasis.
  • Establishment of a diabetic psoriasis-like dermatitis mouse model using imiquimod (IMQ).
  • Treatment of the mouse model with KLF4-overexpressing lentivirus, followed by assessment of metabolic parameters, skin pathology, immune cell infiltration, and inflammatory markers.

Main Results:

  • KLF4 expression was found to be downregulated in patients with T2DM and psoriasis.
  • KLF4 overexpression in the mouse model significantly improved glucose and lipid metabolism.
  • KLF4 overexpression reduced skin erythema, scaling, thickening, psoriasis area severity index (PASI), and mast cell infiltration, while decreasing inflammatory markers.

Conclusions:

  • KLF4 plays a protective role in ameliorating inflammation associated with T2DM and psoriasis.
  • KLF4 exerts its anti-inflammatory effects, at least in part, through modulation of the TIMP3/ADAM17 pathway.
  • KLF4 represents a potential therapeutic target for managing inflammatory skin conditions in diabetic patients.
Keywords:
Inflammatory responseKLF4Macrophage polarizationPsoriasisTIMP3/ADAM17 pathwayType 2 diabetes mellitus

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