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Review
. 2023 Dec 1;13(4S2):e2023314S.
doi: 10.5826/dpc.1304S2a314S.

Aetiopathogenesis of Vitiligo

Katia Boniface  1
Affiliations
Review

Aetiopathogenesis of Vitiligo

Katia Boniface. Dermatol Pract Concept. .

Abstract

Vitiligo is a chronic auto-immune disease characterized by skin depigmentation due to the loss of melanocytes. The better understanding of the disease mechanisms is currently undergoing a significant dynamism, opening a new era in therapeutic development. The pathophysiology of vitiligo has attracted the attention of researchers for years and many advances have been made in clarifying the crosstalk between the cellular players involved in the development of vitiligo lesions. The understanding of the complex interactions between epidermal cells (i.e. melanocytes and keratinocytes), dermal fibroblasts, and immune cells, led to a better characterization of the signals leading to the loss of melanocytes. Recent advances highlighted the role resident T memory cells in the development and recurrence of lesions. This narrative review aims to give an overview of the mechanisms leading to melanocyte disappearance in vitiligo, with a focus on the intercellular interaction network involved in the activation of the local skin immune response.

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Conflict of interest statement

Competing Interests: Katia Boniface received grants from Calypso Biotech, LEO Pharma, Pfizer, Pierre Fabre, Sanofi, and has a patent on MMP9 inhibitors and uses thereof in the prevention or treatment of a depigmenting disorder and three-dimensional model of depigmenting disorder.

Figures

Figure 1
Figure 1
Pathophysiological mechanisms of vitiligo. In a genetically predisposed individual and under environmental triggers, epidermal cells (keratinocytes and melanocytes) will release danger signals (e.g.: HSP70), leading to the activation of the innate immune system. IFNγ-producing innate lymphoid cells (ILC1) or IFNα-producing plasmacytoid dendritic cells will induce the production of chemokines, such as CXCL9, CXCL10, or CXCL16 by epidermal and dermal cells. Melanocytes expressing the CXCR3B subunit can be impacted by the interaction with these ligands. Together, these events will induce local activation of resident memory T cells and the recruitment of circulating T cells expressing CXCR3 and NKG2D and producing elevated levels IFNγ and TNFα, leading to the loss of melanocytes and depigmentation.
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