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已发表论文
整合多组学与实验分析识别TAPBP为连接白癜风遗传易感性与黑素细胞功能障碍的关键介质
Authors Shi J, Guo M, Fu L, He J, Hu Y
Received 29 October 2025
Accepted for publication 20 January 2026
Published 23 January 2026 Volume 2026:19 577486
DOI https://doi.org/10.2147/CCID.S577486
Checked for plagiarism Yes
Review by Single anonymous peer review
Peer reviewer comments 2
Editor who approved publication: Dr Monica K. Li
Jinlong Shi,1,* Mingzhen Guo,2,* Liying Fu,1 Jiangman He,1 Yuan Hu3
1Department of Dermatology, Zhengzhou People’s Hospital, Zhengzhou, Henan, People’s Republic of China; 2Department of Laboratory, Women and Children’s Hospital Affiliated to Qingdao University, Qingdao, Shandong, People’s Republic of China; 3Department of Dermatology, Suining Central Hospital, Suining, Sichuan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yuan Hu, Email huyuanfree@163.com
Background: Vitiligo is an autoimmune depigmenting disorder characterized by selective melanocyte loss; however, the specific molecular bridges between genetic risk variants and melanocyte-intrinsic immune vulnerability remain largely unexplored.
Objective: To elucidate the molecular link between genetic susceptibility and melanocyte injury in vitiligo by integrating multi-omics data.
Methods: We integrated large-scale genome-wide association data (FinnGen R12, n=466,064), expression quantitative trait loci (eQTLgen, n=31,684), and single-cell transcriptomic profiles to identify genes mediating vitiligo susceptibility.
Results: Cross-omic analysis identified TAPBP as a top candidate, which is significantly upregulated in lesional melanocytes and core to the antigen-processing network. Functional validation in human melanocytes demonstrated that TAPBP overexpression significantly increased HLA class I expression, suppressed cell proliferation, and induced apoptosis. Transcription factor analysis further identified STAT2 as a key upstream regulator, linking interferon signaling to aberrant antigen presentation.
Conclusion: These findings suggest that the STAT2–TAPBP axis enhances melanocyte immunogenicity and vulnerability to cytotoxic attack. Our study provides a novel mechanistic link between genetic variation and immune-mediated destruction, positioning TAPBP as a potential biomarker and a target for precision immunotherapy in vitiligo.
Keywords: vitiligo, TAPBP, antigen presentation, multi-omics integration
1Department of Dermatology, Zhengzhou People’s Hospital, Zhengzhou, Henan, People’s Republic of China; 2Department of Laboratory, Women and Children’s Hospital Affiliated to Qingdao University, Qingdao, Shandong, People’s Republic of China; 3Department of Dermatology, Suining Central Hospital, Suining, Sichuan, People’s Republic of China
*These authors contributed equally to this work
Correspondence: Yuan Hu, Email huyuanfree@163.com
Background: Vitiligo is an autoimmune depigmenting disorder characterized by selective melanocyte loss; however, the specific molecular bridges between genetic risk variants and melanocyte-intrinsic immune vulnerability remain largely unexplored.
Objective: To elucidate the molecular link between genetic susceptibility and melanocyte injury in vitiligo by integrating multi-omics data.
Methods: We integrated large-scale genome-wide association data (FinnGen R12, n=466,064), expression quantitative trait loci (eQTLgen, n=31,684), and single-cell transcriptomic profiles to identify genes mediating vitiligo susceptibility.
Results: Cross-omic analysis identified TAPBP as a top candidate, which is significantly upregulated in lesional melanocytes and core to the antigen-processing network. Functional validation in human melanocytes demonstrated that TAPBP overexpression significantly increased HLA class I expression, suppressed cell proliferation, and induced apoptosis. Transcription factor analysis further identified STAT2 as a key upstream regulator, linking interferon signaling to aberrant antigen presentation.
Conclusion: These findings suggest that the STAT2–TAPBP axis enhances melanocyte immunogenicity and vulnerability to cytotoxic attack. Our study provides a novel mechanistic link between genetic variation and immune-mediated destruction, positioning TAPBP as a potential biomarker and a target for precision immunotherapy in vitiligo.
Keywords: vitiligo, TAPBP, antigen presentation, multi-omics integration