Postępy Dermatologii i Alergologii

Abstract

3/2019 vol. 36
Original paper

Evaluation of selected mechanisms of immune tolerance in psoriasis

  1. Department of Dermatology, Sexually Transmitted Diseases and Clinical Immunology, University of Warmia and Mazury, Olsztyn, Poland
Adv Dermatol Allergol 2019; XXXVI (3): 315-324
Online publish date: 2019/06/19
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Introduction

Psoriasis is an autoimmune disease with an excessively aberration of the Th17/Treg balance and deficiency of anti-inflammatory cytokines.

Aim

Evaluation of Treg markers expression in the lesional and perilesional psoriatic skin and serum anti-inflammatory cytokines in male psoriatic patients compared to healthy men.

Material and methods

Treg markers (FoxP3+, CD4, CTLA-4, CD25/IL-2R, CD39/ENTPD1, IL-7R/CD127, CD3) and tissue expression of protective cytokines (IL-10, IL-35, TGF-β) in the lesional and perilesional psoriatic skin from 33 male patients compared to 6 healthy skin samples were evaluated by immunohistochemistry. ELISA was used to assess serum IL-10, IL-35 and TGF-β levels.

Results

The serum levels of IL-35, IL-10 and TGF-β1 were higher in psoriatic patients than in controls but without any statistically significant relationship with PASI. The expressions of IL-35, CD4, IL-10, TGF-β1, CD3, FOXP3 and CD25/IL-2R were varied in different experimental groups (p < 0.05). The level of IL-35 was the lowest in psoriatic lesions (p < 0.05) compared to perilesional skin and to controls. CD4, IL-10 and TGF-β1 expressions were higher (p < 0.05) in perilesional skin than in lesions. TGF-β1 expression was decreased in psoriatic lesions compared to controls (p < 0.05). CD25/IL2R expression was increased in healthy skin compared to psoriatic skin (p < 0.05). FOXP3 expression was elevated in psoriatic skin compared to healthy and perilesional one. There was no difference between experimental groups in CTLA-4, IL7R/CD127 and CD39/ENTPD1 expression.

Conclusions

The differences between the levels of protective cytokines and expression of Treg markers might explain the inflammation development in psoriasis.

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