Psoriasis vulgaris (PsV) is an inflammatory skin disease histologically characterized
by epidermal hyperplasia, inflammatory cell infiltration and vascular changes in which
T-lymphocytes and associated cytokines play a central role [
[1]
]. A dysregulated cutaneous immune response occurs in genetically susceptible individuals
and the features of inflammation are characterized by tumor necrosis factor (TNF)-α
dependence and exaggerated helper T cell 1 (Th1) and 17 (Th17) activation. Interleukin
(IL)-22 is an IL-10 family cytokine member produced by Th17 cells and plays a role
in the promotion of inflammation and tissue repair at barrier surfaces [
[2]
]. IL-22 is required for Th17 cell-mediated pathology in a mouse model of psoriasis-like
skin inflammation [
[3]
], and circulating IL-22 levels are significantly higher in psoriatic patients than
in normal subjects [
4
,
5
]. Atopic dermatitis (AD) is a chronic, relapsing inflammatory skin disease that is
basically considered to be a Th-2 type disease. However, a recent study suggests a
possible role of Th17 cells in AD [
[6]
]. The study has shown that the number of Th17 cells is increased in the peripheral
blood and acute lesional skin of AD and that IL-17 and IL-22 synergistically enhance
the production of IL-8 from keratinocytes [
[6]
]. Since there are few genetic studies of the polymorphisms of IL22 in populations of Asian and European ancestry, we conducted association studies to
assess whether IL22 gene variants contribute to the susceptibility to PsV or AD in a Japanese population.Keywords
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Article info
Publication history
Published online: May 13, 2013
Received:
March 1,
2013
Identification
Copyright
© 2013 Japanese Society for Investigative Dermatology. Published by Elsevier Inc. All rights reserved.
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- Corrigendum to “Genetic polymorphisms in the IL22 gene are associated with psoriasis vulgaris in a Japanese population” [J. Dermatol. Sci. 71 (2013) 148–150]Journal of Dermatological ScienceVol. 74Issue 1
