生物学标志物在白癜风病期监测中的研究进展

doi:10.3969/j.issn.1006-5725.2025.17.023

摘要/Abstract

摘要：

白癜风是一种常见的色素脱失性皮肤病，其临床表现为皮肤或黏膜上的色素减退或脱失斑。准确区分进展期与稳定期对于制定治疗方案至关重要。本综述通过检索和分析相关文献，总结皮损处和外周血中用于监测白癜风病期的潜在生物学标志物及其研究现状。皮损处炎症浸润（如T淋巴细胞数量增加）、趋化因子（如CXCL9、CXCL10）、热休克蛋白70（HSP70）及特定微小RNA（miRNA）的表达变化与白癜风进展期密切相关。外周血中多种细胞因子（如IL-6、IL-17、IFN-γ、TNF-α）和趋化因子（如CXCL10、CCL20）以及特定miRNA（如miR-25）的水平升高也被发现与疾病活动性相关，部分标志物展现出较高的敏感性和特异性。未来研究需深入探索其分子机制、验证临床应用价值并开发更优化的检测方法，有望实现对白癜风活动性的精准评估和监测。

关键词: 白癜风, 生物学, 标志物, 病期

Abstract:

Vitiligo is a common depigmentation skin disorder， characterized by hypopigmented or depigmented patches on the skin or mucous membranes. The disease can be classified into two stages： the active stage and the stable stage. Accurately determining the disease stage is crucial for developing an appropriate treatment plan. However， there is currently no standardized biological marker to assess the disease stage. This article reviews the progress of research on biological markers for different stages of vitiligo.

Key words: vitiligo, biology, markers, disease stage

中图分类号:

R751

曹露,涂海燕,赵阳. 生物学标志物在白癜风病期监测中的研究进展[J]. 实用医学杂志, 2025, 41(17): 2767-2771.

Lu CAO,Haiyan TU,Yang ZHAO. Research progress of biomarkers in the monitoring of vitiligo stages[J]. The Journal of Practical Medicine, 2025, 41(17): 2767-2771.

参考文献 38

[1]	PEREZ-BOOTELLO J， COVA-MARTIN R， NAHARRO-RODRIGUEZ J， et al. Vitiligo： Pathogenesis and New and Emerging Treatments［J］. Int J Mol Sci， 2023， 24（24）：17306. doi:10.3390/ijms242417306 doi: 10.3390/ijms242417306
[2]	RAMOT Y， ROSENBERG V， ZHOU L， et al. Epidemiology and Treatment Patterns of Patients with Vitiligo： A Real-World Analysis［J］. Adv The， 2024， 41（7）：2890-2906. doi:10.1007/s12325-024-02875-0 doi: 10.1007/s12325-024-02875-0
[3]	BELLEI B， PAPACCIO F， PICARDO M. Regenerative Medicine-Based Treatment for Vitiligo： An Overview［J］. Biomedicines， 2022，10（11）：2744. doi:10.3390/biomedicines10112744 doi: 10.3390/biomedicines10112744
[4]	JOGE R R， KATHANE P U， JOSHI S H. Vitiligo： A Narrative Review［J］. Cureus， 2022， 14（9）：e29307.
[5]	曹露，赵阳. 皮肤移植治疗稳定期白癜风的研究进展［J］. 实用医学杂志， 2025，41（2）：300-304.
[6]	YADAV A K， SINGH P， KHUNGER N. Clinicopathologic Analysis of Stable and Unstable Vitiligo： A Study of 66 Cases［J］. Am J Dermatopathol， 2016， 38（8）：608-613. doi:10.1097/dad.0000000000000539 doi: 10.1097/dad.0000000000000539
[7]	ABDALLAH M， LOTFI R， OTHMAN W， et al. Assessment of tissue FoxP3⁺， CD4⁺ and CD8⁺ T-cells in active and stable nonsegmental vitiligo［J］. Int J Dermatol， 2014， 53（8）：940-946. doi:10.1111/ijd.12160 doi: 10.1111/ijd.12160
[8]	STRASSNER J P， RASHIGHI M， AHMED R M， et al. Suction blistering the lesional skin of vitiligo patients reveals useful biomarkers of disease activity［J］. J Am Acad Dermatol， 2017， 76（5）：847-855. doi:10.1016/j.jaad.2016.12.021 doi: 10.1016/j.jaad.2016.12.021
[9]	ZHANG B， LI T， TANG Y， et al. The effects of 308-nm excimer laser on the infiltration of CD4⁺， CD8⁺ T-cells， and regulatory T cells in the lesional skin of patients at active and stable stages of nonsegmental vitiligo［J］. J Dermatolog Treat， 2021， 32（6）：580-584. doi:10.1080/09546634.2019.1687825 doi: 10.1080/09546634.2019.1687825
[10]	NG C Y， CHAN Y P， CHIU Y C， et al. Targeting the elevated IFN-γ in vitiligo patients by human anti- IFN-γ monoclonal antibody hampers direct cytotoxicity in melanocyte［J］. J Dermatol Sci， 2023， 110（3）：78-88. doi:10.1016/j.jdermsci.2023.04.006 doi: 10.1016/j.jdermsci.2023.04.006
[11]	LIN F， HU W， XU W， et al. CXCL9 as a key biomarker of vitiligo activity and prediction of the success of cultured melanocyte transplantation［J］. Sci Rep， 2021， 11（1）：18298. doi:10.1038/s41598-021-97296-2 doi: 10.1038/s41598-021-97296-2
[12]	MARCHIORO H Z， SILVA DE CASTRO C C， FAVA V M， et al. Update on the pathogenesis of vitiligo［J］. An Bras Dermatol， 2022，97（4）：478-490. doi:10.1016/j.abd.2021.09.008 doi: 10.1016/j.abd.2021.09.008
[13]	DOSS R W， EL-RIFAIE A A， ABDEL-WAHAB A M， et al. Heat Shock Protein-70 Expression in Vitiligo and its Relation to the Disease Activity［J］. Indian J Dermatol， 2016， 61（4）：408-412. doi:10.4103/0019-5154.185704 doi: 10.4103/0019-5154.185704
[14]	OCHOA-RAMÍREZ L A， DÍAZ-CAMACHO S P， MELLADO-CORRALES S N， et al. Analysis of the heat shock protein 70 （HSP70） genetic variants in nonsegmental vitiligo patients［J］. Int J Dermatol， 2023， 62（2）：225-230. doi:10.1111/ijd.16487 doi: 10.1111/ijd.16487
[15]	FEGHAHATI F S， GHAFOURI-FARD S. A comprehensive outline of the role of non-coding RNAs in vitiligo［J］. Biochem Biophys Rep， 2025，41：101916. doi:10.1016/j.bbrep.2025.101916 doi: 10.1016/j.bbrep.2025.101916
[16]	ŠAHMATOVA L， TANKOV S， PRANS E， et al. MicroRNA-155 is Dysregulated in the Skin of Patients with Vitiligo and Inhibits Melanogenesis-associated Genes in Melanocytes and Keratinocytes［J］. Acta Derm Venereol， 2016，96（6）：742-747.
[17]	BRAHMBHATT H D， GUPTA R， GUPTA A， et al. The long noncoding RNA MALAT1 suppresses miR-211 to confer protection from ultraviolet-mediated DNA damage in vitiligo epidermis by upregulating sirtuin 1［J］. Br J Dermatol， 2021， 184（6）：1132-1142. doi:10.1111/bjd.19666 doi: 10.1111/bjd.19666
[18]	MANSURI M S， SINGH M， DWIVEDI M， et al. MicroRNA profiling reveals differentially expressed microRNA signatures from the skin of patients with nonsegmental vitiligo［J］. Br J Dermatol， 2014， 171（5）：1263-1267. doi:10.1111/bjd.13109 doi: 10.1111/bjd.13109
[19]	ABDALLAH M， EL-MOFTY M， ANBAR T， et al. CXCL-10 and Interleukin-6 are reliable serum markers for vitiligo activity： A multicenter cross-sectional study［J］. Pigment Cell Melanoma Res， 2018， 31（2）：330-336. doi:10.1111/pcmr.12667 doi: 10.1111/pcmr.12667
[20]	UTTMANI B M， ADYA K A， INAMADAR A C. Serum interleukin-6 and high sensitivity C-reactive protein levels and their correlation with the vitiligo disease activity and extent： A cross-sectional study of 58 patients［J］. J Cutan Aesthet Surg， 2024， 17（3）：266-271.
[21]	BELPAIRE A， VAN GEEL N， SPEECKAERT R. From IL-17 to IFN-γ in inflammatory skin disorders： Is transdifferentiation a potential treatment target？［J］. Front Immunol， 2022， 13：932265. doi:10.3389/fimmu.2022.932265 doi: 10.3389/fimmu.2022.932265
[22]	BERNARDINI N， SKROZA N， TOLINO E， et al. IL-17 and its role in inflammatory， autoimmune， and oncological skin diseases： state of art［J］. Int J Dermatol， 2020，59（4）：406-411. doi:10.1111/ijd.14695 doi: 10.1111/ijd.14695
[23]	NIERADKO-IWANICKA B， PRZYBYLSKA D， BORZĘCKI A. A case-control study on immunologic markers of patients with vitiligo［J］. Biomed Pharmacother， 2022， 156：113785. doi:10.1016/j.biopha.2022.113785 doi: 10.1016/j.biopha.2022.113785
[24]	TOMASZEWSKA K， KOZŁOWSKA M， KASZUBA A， et al. Increased Serum Levels of IFN-γ， IL-1β， and IL-6 in Patients with Alopecia Areata and Nonsegmental Vitiligo［J］. Oxid Med Cell Longev， 2020， 2020：5693572. doi:10.1155/2020/5693572 doi: 10.1155/2020/5693572
[25]	CUSTURONE P， DI BARTOLOMEO L， IRRERA N， et al. Role of Cytokines in Vitiligo： Pathogenesis and Possible Targets for Old and New Treatments［J］. Int J Mol Sci， 2021，22（21）：11429. doi:10.3390/ijms222111429 doi: 10.3390/ijms222111429
[26]	MAI Z M， BYRNE S N， LITTLE M P， et al. Solar UVR and Variations in Systemic Immune and Inflammation Markers［J］. JID Innov， 2021， 1（4）：100055. doi:10.1016/j.xjidi.2021.100055 doi: 10.1016/j.xjidi.2021.100055
[27]	HOSSAIN M R， ANSARY T M， KOMINE M， et al. Diversified Stimuli-Induced Inflammatory Pathways Cause Skin Pigmentation［J］. Int J Mol Sci， 2021， 22（8）：3970. doi:10.3390/ijms22083970 doi: 10.3390/ijms22083970
[28]	YANG L， YANG S， LEI J， et al. Role of chemokines and the corresponding receptors in vitiligo： A pilot study［J］. J Dermatol， 2018， 45（1）：31-38. doi:10.1111/1346-8138.14004 doi: 10.1111/1346-8138.14004
[29]	WANG X X， WANG Q Q， WU J Q， et al. Increased expression of CXCR3 and its ligands in patients with vitiligo and CXCL10 as a potential clinical marker for vitiligo［J］. Br J Dermatol， 2016， 174（6）：1318-1326. doi:10.1111/bjd.14416 doi: 10.1111/bjd.14416
[30]	ZHANG L， KANG Y， CHEN S， et al. Circulating CCL20： A potential biomarker for active vitiligo together with the number of Th1/17 cells［J］. J Dermatol Sci， 2019， 93（2）：92-100. doi:10.1016/j.jdermsci.2018.12.005 doi: 10.1016/j.jdermsci.2018.12.005
[31]	RICHMOND J M， MASTERJOHN E， CHU R， et al. CXCR3 Depleting Antibodies Prevent and Reverse Vitiligo in Mice［J］. J Invest Dermatol， 2017， 137（4）：982-985. doi:10.1016/j.jid.2016.10.048 doi: 10.1016/j.jid.2016.10.048
[32]	AULAKH S， GOEL S， KAUR L， GULATI S， et al. Differential expression of serum CXCL9 and CXCL10 levels in vitiligo patients and their correlation with disease severity and stability： A cross-sectional study［J］. Indian J Dermatol Venereol Leprol， 2025， 91（1）：9-15. doi:10.25259/ijdvl_793_2023 doi: 10.25259/ijdvl_793_2023
[33]	ERDOĞAN A， MUTLU H S， SOLAKOĞLU S. Autologously transplanted dermis-derived cells alleviated monobenzone-induced vitiligo in mouse［J］. Exp Dermatol， 2022， 31（9）：1355-1363. doi:10.1111/exd.14603 doi: 10.1111/exd.14603
[34]	CHALLA A， CHAUHAN S， PANGTI R， et al. Evaluation of clinical efficacy and laboratory indicators of non-cultured epidermal cell suspension and hair follicle cell suspension in surgical management of stable vitiligo： A randomized comparative trial［J］. J Cosmet Dermatol， 2022， 21（12）：6958-6964. doi:10.1111/jocd.15407 doi: 10.1111/jocd.15407
[35]	KAWAKAMI T. Surgical procedures and innovative approaches for vitiligo regenerative treatment and melanocytorrhagy［J］. J Dermatol， 2022， 49（4）：391-401. doi:10.1111/1346-8138.16316 doi: 10.1111/1346-8138.16316
[36]	HUO J， LIU T， LI F， et al. MicroRNA‑21‑5p protects melanocytes via targeting STAT3 and modulating Treg/Teff balance to alleviate vitiligo［J］. Mol Med Rep， 2021， 23（1）：51. doi:10.3892/mmr.2020.11689 doi: 10.3892/mmr.2020.11689
[37]	AGUENNOUZ M， GUARNERI F， OTERI R， et al. Serum levels of miRNA-21-5p in vitiligo patients and effects of miRNA-21-5p on SOX5， beta-catenin， CDK2 and MITF protein expression in normal human melanocytes［J］. J Dermatol Sci， 2021， 101（1）：22-29. doi:10.1016/j.jdermsci.2020.10.014 doi: 10.1016/j.jdermsci.2020.10.014
[38]	SHI Q， ZHANG W， GUO S， et al. Oxidative stress-induced overexpression of miR-25： The mechanism underlying the degeneration of melanocytes in vitiligo［J］. Cell Death Differ， 2016， 23（3）：496-508. doi:10.1038/cdd.2015.117 doi: 10.1038/cdd.2015.117