@Article{ecn.2011.0294,
AUTHOR = {Anna Michalak-Stoma, Aldona Pietrzak, Jacek C. Szepietowski, Anna Zalewska-Janowska, Tomasz Paszkowski, Grazyna Chodorowska˙},
TITLE = {Cytokine network in psoriasis revisited},
JOURNAL = {European Cytokine Network},
VOLUME = {22},
YEAR = {2011},
NUMBER = {4},
PAGES = {160--168},
URL = {http://www.techscience.com/ECN/v22n4/65813},
ISSN = {1952-4005},
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.},
DOI = {10.1684/ecn.2011.0294}
}