Immune Imbalance Drives Keloid Pathogenesis: Emerging Targets for Precision Immunotherapy

Area of Science:

• Dermatology
• Immunology
• Pathogenesis of Scarring Disorders

Background:

• Keloids are characterized by fibroblast hyperactivity and excessive extracellular matrix deposition.
• Emerging research highlights immune dysregulation as a key driver of keloid formation and persistence.
• Specific immune cells (M2 macrophages, mast cells, T-cell subsets) and cytokines create a pro-fibrotic microenvironment.

Purpose of the Study:

• To review the role of immune dysregulation in keloid pathogenesis.
• To explore novel immune-targeted therapeutic strategies for keloids.
• To identify challenges and future directions in keloid research and treatment.

Main Methods:

• Review of multi-omics and single-cell analyses of keloid tissue.
• Analysis of key signaling pathways involved in keloid formation.
• Evaluation of emerging and experimental immune-modulating therapies.

Main Results:

• Immune cell infiltration and altered cytokine profiles are central to keloid pathogenesis.
• Signaling pathways like TGF-β, IL-4/IL-13, and IL-6 are implicated in a self-perpetuating fibrotic loop.
• Soluble human leukocyte antigen-E and tissue-resident memory T cells are potential biomarkers for recurrence.

Conclusions:

• Immune dysregulation is a critical factor in keloid development and recurrence.
• Targeting immune pathways, such as IL-4/IL-13 with Dupilumab, shows therapeutic promise.
• Further research with validated models and trials is needed for personalized keloid immunotherapy.