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Updated: Jan 21, 2026

The Goeckerman Regimen for the Treatment of Moderate to Severe Psoriasis
Published on: July 11, 2013
Evaluation of selected mechanisms of immune tolerance in psoriasis
Agnieszka Owczarczyk-Saczonek1, Joanna Czerwińska1, Małgorzata Orylska1
1Department of Dermatology, Sexually Transmitted Diseases and Clinical Immunology, University of Warmia and Mazury, Olsztyn, Poland.
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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