Open Access

REVIEW

Cytokine network in psoriasis revisited

Anna Michalak-Stoma¹, Aldona Pietrzak¹, Jacek C. Szepietowski², Anna Zalewska-Janowska³, Tomasz Paszkowski⁴, Grazyna Chodorowska˙ ¹

1 Department of Dermatology, Venereology and Paediatric Dermatology, Medical University of Lublin, ul. Radziwiłłowska 13, 20-080 Lublin, Poland
2 Department of Dermatology, Venereology and Allergology, Medical University of Wrocław, ul. Chałubińskiego 1, 50-368 Wrocław, Poland
3 Psychodermathology Department, Chair of Clinical Immunology and Microbiology, Medical University of Łódź, ul. Pomorska 251, 92-213 Łódź, Poland
4 III Department of Gynecology, Medical University of Lublin, ul. Jaczewskiego 8, 20-094 Lublin, Poland

* Corresponding Author: Anna Michalak-Stoma,

European Cytokine Network 2011, 22(4), 160-168. https://doi.org/10.1684/ecn.2011.0294

Accepted 30 September 2011;

Abstract

Psoriasis is a chronic genetically determined, erythemato-squamous disease associated with many comorbidities. Evidence from clinical studies and experimental models support the concept that psoriasis is a T cell-mediated inflammatory skin disease and T helper (Th) cells – Th1, Th17 and Th22 – play an important role in the pathogenesis. Th1 cytokines IFNγ, IL-2, as well as Th17 cytokines IL-17A, IL-17F, IL-22, IL-26, and TNFα (Th1 and Th17 cytokine) are increased in serum and lesional skin. IL-22 produced by Th17 and new subset of T helper cells, Th22, is also increased within psoriatic lesions and in the serum. Other recently recognized cytokines of significant importance in psoriasis are IL-23, IL-20 and IL-15. The IL-23/Th17 pathway plays a dominant role in psoriasis pathogenesis. Currently due to enormous methodological progress, more and more clinical and histopathological psoriatic features could be explained by particular cytokine imbalance, which still is one of the most fascinating dermatological research fields stimulating new and new generations of researchers.

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