Distribution of melanocytes in the skin of psoriasis patients

Cover Page

Cite item


Psoriasis is a chronic immune-mediated inflammatory disease with predominant damage to the skin and joints. Despite fundamental studies of its pathogenesis, the cause of the development of the T-cell response has not been determined. More recently, a new concept has been proposed for the formation of psoriatic inflammation, where a significant role in the pathogenesis is assigned to melanocytes. Evaluation of the content of these cells and their relationship with other participants of inflammation will allow expanding the understanding of the pathogenesis of psoriasis and the targets of targeted therapy.

Aim: study of the quantity, distribution and proliferative activity of melanocytes.

Materials and methods. The study included 20 patients with plaque psoriasis: men — 18 (90 %), women — 2 (10 %). The severity of the disease was assessed by the index of the area and severity of PASI psoriatic lesions. In the histological specimens, the thickness of the epidermis, the length of the basement membrane in the visual field, and pathological changes in the epidermis and dermis were determined. For immunohistochemical detection of melanocytes, the MelanA marker was used, the cell proliferative activity was Ki67, and the cytotoxic T-lymphocytes, CD8. Used a dual visualization system. Differences were considered significant at p < 0.05.

Results. The number of MelanAcells in the affected skin of patients with psoriasis — 54 (44–64)/1.4 mm2 was 2.4 times higher than in unaffected skin — 24 (22–30)/1.4 mm2 (p < 0.05), and 2 times higher than in the skin of healthy individuals — 27 (25–32)/1.4 mm2 (p < 0.05). The content of MelanA+ cells per 1 mm of the basement membrane in patients with psoriasis in the affected skin is 11 [7–13] cells/mm, unaffected — 12 [11–14] cells/mm and in healthy individuals — 12 [9–13] cells/mm did not significantly differ (p > 0.05). In the affected skin of patients with psoriasis, multiple contacts of CD8+ and MelanA+ cells were detected — 10 [8–13]/1.4 mm2.

Conclusions. In the affected skin of patients with psoriasis, the absolute number of melanocytes is significantly higher than in unaffected skin and the skin of healthy individuals, while the ratio of melanocytes to basal keratinocytes did not differ. In the skin of all the studied groups, no melanocytes in the proliferation stage were detected. Multiple contacts of MelanA+ and CD8+ cells are observed in the affected skin of patients with psoriasis.

Conflict of interest: the authors state that there is no potential conflict of interest requiring disclosure in this article.

About the authors

A. S. Zhukov

S. M. Kirov Military Medical Academy, Ministry of Defence of the Russian Federation

Author for correspondence.
Email: doctor-vma@mail.ru
Aleksander S. Zhukov — Cand. Sci. (Med.), Doctoral Candidate, Department of Skin and Sexually Transmitted Diseases Russian Federation

V. R. Khairutdinov

S. M. Kirov Military Medical Academy, Ministry of Defence of the Russian Federation

Email: haric03@list.ru
Vladislav R. Khairutdinov — Dr. Sci. (Med.)., Assoc. Prof., Assoc. Prof. of the Department of Skin and Sexually Transmitted Diseases Russian Federation

I. E. Belousova

S. M. Kirov Military Medical Academy, Ministry of Defence of the Russian Federation

Email: irena.belousova@mail.ru
Irena E. Belousova — Dr. Sci. (Med.)., Assoc. Prof., Prof. of the Department of Skin and Sexually Transmitted Diseases Russian Federation

A. V. Samtsov

S. M. Kirov Military Medical Academy, Ministry of Defence of the Russian Federation

Email: avsamtsov@mail.ru
Aleksey V. Samtsov — Dr. Sci. (Med.)., Prof., Head of the Department of Skin and Sexually Transmitted Diseases Russian Federation


  1. Aggarwal S., Nayek A., Pradhan D. et al. dbGAPs: A comprehensive database of genes and genetic markers associated with psoriasis and its subtypes. Genomics. 2017;(17):30115–30125.
  2. Dand N., Duckworth M., Baudry D. et al. BADBIR Study Group; BSTOP Study Group; PSORT Consortium. HLA-C*06:02 genotype is a predictive biomarker of biologic treatment response in psoriasis. J Allergy Clin Immunol. 2019;143(6):2120–2130.
  3. Хайрутдинов В. Р., Жуков А. С., Пономарев И. А. и др. Роль полиморфных генов программируемой клеточной гибели в формировании риска развития псориаза. Вестник дерматологии и венерологии. 2009;4:4–8.
  4. Хайрутдинов В. Р. Генетический паспорт больного псориазом. Вестник дерматологии и венерологии. 2011;4:14–19.
  5. Mabuchi T., Ota T., Manabe Y. et al. HLA-C*12:02 is a susceptibility factor in late-onset type of psoriasis in Japanese. J Dermatol. 2014;41:697–704.
  6. Prinz J. C. Human Leukocyte Antigen-Class I Alleles and the Autoreactive T Cell Response in Psoriasis Pathogenesis. Front Immunol. 2018;30(9):954–959.
  7. Arakawa A., Siewert K., Stöhr J. et al. Melanocyte antigen triggers autoimmunity in human psoriasis. J Exp Med. 2015;212(13):2203–2212.
  8. Bonifacio K. M., Kunjravia N., Krueger J. G., Fuentes-Duculan J. Cutaneous expression of a disintegrin-like and metalloprotease domain containing thrombospondin type 1 motif- like 5 (ADAMTSL5) in psoriasis goes beyond melanocytes. J Pigment Disord. 2016;3(3):515–521.
  9. Shah P. P., Desai P. R., Boakye C. H. et al. Percutaneous delivery of α-melanocyte-stimulating hormone for the treatment of imiquimod-induced psoriasis. J Drug Target. 2016;24(6):537–547.
  10. Brajac I., Kastelan M., Prpić-Massari L. et al. Melanocyte as a possible key cell in the pathogenesis of psoriasis vulgaris. Med Hypotheses. 2009;73(2):254–256.
  11. Tobin D. J., Paus R. Graying: Gerontobiology of the hair follicle pigmentary unit. Exp Gerontol. 2001;36(1):29–54.
  12. Strassner J. P., Rashighi M., Harris J. E. Melanocytes in psoriasis: convicted culprit or bullied bystander? Pigment Cell Melanoma Res. 2016;29(3):261–263.
  13. Nystedt S. Molecular cloning of a potential proteinase activated receptor. Proc Natl Acad Sci USA. 1994;91(20):9208–9212.
  14. Scott G. Protease-activated receptor 2, a receptor involved in melanosome transfer, is upregulated in human skin by ultraviolet irradiation. J Invest Dermatol. 2001;117(6):1412–1420.
  15. Yu S., Lan C. E., Yu H. S. Mechanisms of repigmentation induced by photobiomodulation therapy in vitiligo. Exp Dermatol. 2019 Feb;28 Suppl 1:10–14.

Copyright (c) 2019 Zhukov A.S., Khairutdinov V.R., Belousova I.E., Samtsov A.V.

Creative Commons License
This work is licensed under a Creative Commons Attribution 4.0 International License.

СМИ зарегистрировано Федеральной службой по надзору в сфере связи, информационных технологий и массовых коммуникаций (Роскомнадзор).
Регистрационный номер и дата принятия решения о регистрации СМИ: серия ПИ № ФС 77 - 60448 от 30.12.2014.

This website uses cookies

You consent to our cookies if you continue to use our website.

About Cookies