Damage-associated molecular patterns in vitiligo: igniter fuse from oxidative stress to melanocyte loss

Jingying Wang, Yinghao Pan, Guangmin Wei, Hanxiao Mao, Rulan Liu, Yuanmin He, Jingying Wang, Yinghao Pan, Guangmin Wei, Hanxiao Mao, Rulan Liu, Yuanmin He

Abstract

Objectives: The pathogenesis of vitiligo remains unclear. In this review, we comprehensively describe the role of damage associated molecular patterns (DAMPs) during vitiligo pathogenesis.

Methods: Published papers on vitiligo, oxidative stress and DAMPs were collected and reviewed via database searching on PubMed, MEDLINE and Embase, etc.

Results: Oxidative stress may be an important inducer of vitiligo. At high oxidative stress levels, damage-associated molecular patterns (DAMPs) are released from keratinocytes or melanocytes in the skin and induce downstream immune responses during vitiligo. Treatment regimens targeting DAMPs can effectively improve disease severity.

Discussion: DAMPs play key roles in initiating host defenses against danger signals, deteriorating the condition of vitiligo. DAMP levels in serum and skin may be used as biomarkers to indicate vitiligo activity and prognosis. Targeted therapies, incorporating HMGB1, Hsp70, and IL-15 could significantly improve disease etiology. Thus, novel strategies could be identified for vitiligo treatment by targeting DAMPs.

Keywords: Adenosine triphosphate (ATP); Antimicrobial peptides (AMPs); Heat shock protein 70 (Hsp70); High mobility group box 1 (HMGB1); Interleukin; S100B; Vitiligo; damage-associated molecular patterns; oxidative stress; pathogenesis.

Conflict of interest statement

No potential conflict of interest was reported by the author(s).

Figures

Figure 1.
Figure 1.
Oxidative stress promotes damage-associated molecular pattern secretion, including HMGB1, HSP70, S100B, ATP, the interleukins, and AMPs. These molecules increase cytokine release and accelerate melanocyte death. Abbreviations: HMGB1, high mobility group box 1; HSP70, heat shock protein 70; ATP, adenosine triphosphate; AMPs, antimicrobial peptides. ROS, reactive oxygen species; ERK, extracellular regulated protein kinase; NF-κB, nuclear factor kappa-B; NLRP3, the NOD-like receptor thermal protein domain associated protein 3; pDC, plasmacytoid dendritic cells.

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