Increased Circulatory Interleukin-17A Levels in Patients with Progressive and Leukotrichial Vitiligo

Overview

Journal Dermatol Res Pract

Publisher Wiley

Specialty Dermatology

Date 2021 May 10

PMID 33968147

Citations 5

Authors

Thai Van Thanh Le

Huy Ngoc Phan

Tran Ngoc Dang

Le Duy Pham

Affiliations

Soon will be listed here.

Abstract

Background: Vitiligo is a chronic condition characterized by skin depigmentation. Although not life-threatening, it significantly impacts quality of life. The pathophysiology of vitiligo remains poorly understood, and treatment options are limited. Mounting evidence supports the importance of autoreactive T cells and, particularly interleukin-17A- (IL-17A-) secreting Th17 cells, in vitiligo. IL-17A targeting has been proven successful in various inflammatory dermatological conditions, including psoriasis and lupus erythematosus.

Objective: We evaluated the relationship between serum levels of IL-17A and the clinicopathological characteristics of Vietnamese vitiligo patients.

Methods: In this cross-sectional study, we analyzed data from 52 nonsegmental vitiligo patients and 50 age- and sex-matched healthy individuals. Serum levels of IL-17A were measured using an enzyme-linked immunosorbent assay. We evaluated the correlation between IL-17A levels and clinical characteristics including leukotrichia, disease duration, vitiligo activity, and body surface area involvement.

Results: Patients with progressive vitiligo had significantly higher IL-17A levels than patients with stable vitiligo ( = 0.014) or healthy individuals ( = 0.002). In addition, serum IL-17A levels were higher in vitiligo patients with leukotrichia than in patients without it ( = 0.04). Furthermore, serum IL-17A levels were negatively correlated with age ( = -0.39, = 0.004) and age of onset ( = -0.33, = 0.016) in vitiligo patients.

Conclusions: Higher serum levels of IL-17A in patients with progressive vitiligo and leukotrichia suggest a potential role of IL-17A in melanocyte destruction in the epidermis and the follicular matrix.

Citing Articles

Vitiligo: From mechanisms of disease to treatable pathways.

Pathak G, J Tan I, Bai G, Dhillon J, Rao B Skin Health Dis. 2024; 4(6):e460.

PMID: 39624766 PMC: 11608881. DOI: 10.1002/ski2.460.

Markers of Metabolic Abnormalities in Vitiligo Patients.

Papaccio F, Ottaviani M, Truglio M, DArino A, Caputo S, Pacifico A Int J Mol Sci. 2024; 25(18).

PMID: 39337683 PMC: 11432710. DOI: 10.3390/ijms251810201.

Vitamin D and Interleukin-17: Are These Serum Biomarkers Useful in Non-Segmental Vitiligo? A Case Control Study from Central India.

George C, Chhabra N, Patel S Indian J Dermatol. 2024; 68(6):725.

PMID: 38371538 PMC: 10869005. DOI: 10.4103/ijd.ijd_442_23.

The role of aryl hydrocarbon receptor in vitiligo: a review.

Li Y, Zeng Y, Chen Z, Tan X, Mei X, Wu Z Front Immunol. 2024; 15:1291556.

PMID: 38361944 PMC: 10867127. DOI: 10.3389/fimmu.2024.1291556.

Vitiligo, from Pathogenesis to Therapeutic Advances: State of the Art.

Diotallevi F, Gioacchini H, De Simoni E, Marani A, Candelora M, Paolinelli M Int J Mol Sci. 2023; 24(5).

PMID: 36902341 PMC: 10003418. DOI: 10.3390/ijms24054910.

References

van den Boorn J, Konijnenberg D, Dellemijn T, van der Veen J, Bos J, Melief C . Autoimmune destruction of skin melanocytes by perilesional T cells from vitiligo patients. J Invest Dermatol. 2009; 129(9):2220-32. DOI: 10.1038/jid.2009.32. View

Okamoto T, Irie R, Fujii S, Huang S, Nizze A, Morton D . Anti-tyrosinase-related protein-2 immune response in vitiligo patients and melanoma patients receiving active-specific immunotherapy. J Invest Dermatol. 1998; 111(6):1034-9. DOI: 10.1046/j.1523-1747.1998.00411.x. View

Frisoli M, Harris J . Vitiligo: Mechanistic insights lead to novel treatments. J Allergy Clin Immunol. 2017; 140(3):654-662. DOI: 10.1016/j.jaci.2017.07.011. View

Le Poole I, van den Wijngaard R, Westerhof W, Das P . Presence of T cells and macrophages in inflammatory vitiligo skin parallels melanocyte disappearance. Am J Pathol. 1996; 148(4):1219-28. PMC: 1861531. View

Swope V, Abdel-Malek Z, Kassem L, Nordlund J . Interleukins 1 alpha and 6 and tumor necrosis factor-alpha are paracrine inhibitors of human melanocyte proliferation and melanogenesis. J Invest Dermatol. 1991; 96(2):180-5. DOI: 10.1111/1523-1747.ep12460991. View

Tembhre M, Sharma V, Sharma A, Chattopadhyay P, Gupta S . T helper and regulatory T cell cytokine profile in active, stable and narrow band ultraviolet B treated generalized vitiligo. Clin Chim Acta. 2013; 424:27-32. DOI: 10.1016/j.cca.2013.05.005. View

Muranski P, Boni A, Antony P, Cassard L, Irvine K, Kaiser A . Tumor-specific Th17-polarized cells eradicate large established melanoma. Blood. 2008; 112(2):362-73. PMC: 2442746. DOI: 10.1182/blood-2007-11-120998. View

Singh S, Zhang H, Foley J, Hedrick M, Farber J . Human T cells that are able to produce IL-17 express the chemokine receptor CCR6. J Immunol. 2007; 180(1):214-21. DOI: 10.4049/jimmunol.180.1.214. View

Acharya P, Mathur M . Interleukin-17 level in patients with vitiligo: A systematic review and meta-analysis. Australas J Dermatol. 2020; 61(2):e208-e212. DOI: 10.1111/ajd.13233. View

10.

Boissy R, Manga P . On the etiology of contact/occupational vitiligo. Pigment Cell Res. 2004; 17(3):208-14. DOI: 10.1111/j.1600-0749.2004.00130.x. View

11.

Garbelli S, Mantovani S, Palermo B, Giachino C . Melanocyte-specific, cytotoxic T cell responses in vitiligo: the effective variant of melanoma immunity?. Pigment Cell Res. 2005; 18(4):234-42. DOI: 10.1111/j.1600-0749.2005.00244.x. View

12.

Alikhan A, Felsten L, Daly M, Petronic-Rosic V . Vitiligo: a comprehensive overview Part I. Introduction, epidemiology, quality of life, diagnosis, differential diagnosis, associations, histopathology, etiology, and work-up. J Am Acad Dermatol. 2011; 65(3):473-491. DOI: 10.1016/j.jaad.2010.11.061. View

13.

Hamarat E, Thompson D, Zabrucky K, Steele D, Matheny K, Aysan F . Perceived stress and coping resource availability as predictors of life satisfaction in young, middle-aged, and older adults. Exp Aging Res. 2001; 27(2):181-96. DOI: 10.1080/036107301750074051. View

14.

Schroder J, Gregory H, Young J, Christophers E . Neutrophil-activating proteins in psoriasis. J Invest Dermatol. 1992; 98(2):241-7. DOI: 10.1111/1523-1747.ep12556058. View

15.

Kruger C, Schallreuter K . A review of the worldwide prevalence of vitiligo in children/adolescents and adults. Int J Dermatol. 2012; 51(10):1206-12. DOI: 10.1111/j.1365-4632.2011.05377.x. View

16.

Antelo D, Filgueira A, Cunha J . Reduction of skin-homing cytotoxic T cells (CD8+ -CLA+) in patients with vitiligo. Photodermatol Photoimmunol Photomed. 2011; 27(1):40-4. DOI: 10.1111/j.1600-0781.2010.00563.x. View

17.

Speeckaert R, Speeckaert M, de Schepper S, van Geel N . Biomarkers of disease activity in vitiligo: A systematic review. Autoimmun Rev. 2017; 16(9):937-945. DOI: 10.1016/j.autrev.2017.07.005. View

18.

Ongenae K, van Geel N, Naeyaert J . Evidence for an autoimmune pathogenesis of vitiligo. Pigment Cell Res. 2003; 16(2):90-100. DOI: 10.1034/j.1600-0749.2003.00023.x. View

19.

Basak P, Adiloglu A, Ceyhan A, Tas T, Akkaya V . The role of helper and regulatory T cells in the pathogenesis of vitiligo. J Am Acad Dermatol. 2008; 60(2):256-60. DOI: 10.1016/j.jaad.2008.09.048. View

20.

Khan R, Gupta S, Sharma A . Circulatory levels of T-cell cytokines (interleukin [IL]-2, IL-4, IL-17, and transforming growth factor-β) in patients with vitiligo. J Am Acad Dermatol. 2012; 66(3):510-1. DOI: 10.1016/j.jaad.2011.07.018. View