Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
Interleukin-22, a TH17 cytokine, mediates IL-23-induced dermal inflammation and acanthosis
Nature 445: 648-651 (2007)
Speaker: 林建達 Time: 2007/04/11 14:00-15:00
Commentator: 王德華 老師 Place: Room 601
Abstract:
Psoriasis is believed to be an immune-mediated disease which affects the skin and joints. It commonly causes red scaly patches to appear on the skin. The disorder is a chronic recurring condition which varies in severity from minor localized patches to complete body coverage. The clinical and histological appearance of stable chronic psoriatic plaques was characterized by hyperplasia of the epidermis (acanthosis), infiltration of leukocytes
into both the dermis and epidermis, and dilation and growth of blood vessels. However, the cause of psoriasis is largely unknown. Recently, interleukin (IL)-23, a cytokine in the development of IL-17-producing T helper cells (TH17 cells), has been shown to be involved in many autoimmune diseases. It is implicated in the pathogenesis of psoriasis. In this paper, the authors showed that IL-22 was preferentially produced by TH17 cells and mediated acanthosis induced by IL-23. IL-22 belongs to the IL-10 family of cytokines and elevated levels of IL-22 are found in the blood of psoriatic patients. Furthermore, IL-22 mediates IL-23-induced acanthosisand dermal inflammation through the activation of Stat3 (signal transduction and activators of transcription 3) in vivo. The TH17 cells, through the production of both IL-22 and IL-17, might have essential functions in host defence and in the pathogenesis of autoimmune diseases such as psoriasis. This recently characterized TH17 pathway, in addition to the TH1 pathway, may provide
new therapeutic targets for the treatment of psoriasis.
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