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Single-Cell Transcriptomic Analysis Reveals an Inflammatory Antigen-Presenting Macrophages Subtype Drive Vitiligo

Ruozhou Qi¹, Min Huang¹, Ziyi Lin¹

¹Department of Dermatology, Dongzhimen Hospital, Beijing University of Chinese Medicine, Beijing, China, bucm.edu.cn.

Mediators of Inflammation

|March 24, 2026

Summary

This study identifies a new inflammatory macrophage subpopulation that drives vitiligo by harming melanocytes and boosting T-cell responses. STAT1 inhibition offers a potential therapeutic strategy for vitiligo.

Area of Science:

Immunology
Dermatology
Single-cell genomics

Background:

Vitiligo is a depigmentation disorder with T-cell involvement, but macrophage roles are unclear.
This study investigates macrophage heterogeneity and function in vitiligo pathogenesis.

Purpose of the Study:

To characterize macrophage subpopulations in vitiligo skin.
To elucidate the functional role of identified macrophages in melanocyte loss and T-cell activation.
To identify key regulatory molecules for therapeutic targeting.

Main Methods:

Single-cell RNA sequencing (scRNA-seq) of vitiligo and healthy skin.
Computational analyses including clustering, pseudotime, cell-cell communication, and hdWGCNA.
In vivo and in vitro experiments to assess STAT1 inhibition effects.

Main Results:

Identified a novel inflammatory antigen-presenting macrophage (Mac-InflamAP) subpopulation enriched in vitiligo lesions.
Mac-InflamAP promotes melanocyte loss via TNF signaling and enhances T-cell antigen presentation.
STAT1 was identified as a key regulator in Mac-InflamAP; its inhibition ameliorated vitiligo progression in vivo.

Conclusions:

An uncharacterized inflammatory macrophage subpopulation drives vitiligo pathogenesis.
STAT1 is a crucial regulator, presenting a potential therapeutic target for vitiligo treatment.
Findings deepen the understanding of immune mechanisms underlying vitiligo.

Keywords:

STAT1 macrophages melanocytes single-cell RNA sequencing vitiligo

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