This review demonstrates immune dysregulation's role in keloids, highlighting macrophages and cytokine secretion's impact on scar formation.
Keloid, as a skin fibrotic proliferative disorder, have a complex pathogenesis that remains incompletely understood. It is characterized by abnormal and excessive scar formation following skin injury. The occurrence and development of keloids are closely associated with immune dysregulation. Immune cells, such as T cells, macrophages, mast cells, and Langerhans cells, play crucial roles in the formation of keloids. These immune cells contribute to keloid initiation and progression through mechanisms including cytokine secretion, promotion of inflammatory responses, and regulation of fibroblast proliferation and collagen synthesis. With advances in immunological research, the roles of fibroblasts, keratinocytes and melanocytes in the immunological dysregulation underlying keloids have received increasing attention. This paper aims to review recent progress on the abnormal immunological regulation involving these three epidermal cell types, in order to provide new insights and theoretical foundations for the treatment of this disease.
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Yuan et al. (2025) studied this question.
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