Abstract：
:Psoriasis is a complex inflammatory process resulting from activation of the well-defined interleukin (IL)-23/T17 cytokine axis. We review the role of key cytokines IL-17 and IL-23 in psoriasis, as well as tumor necrosis factor (TNF)α, focusing on therapeutic cytokine interventions and what they reveal about psoriatic inflammation. The potential role of recently described epidermal IL-36RN and CARD14 genetic mutations in psoriasis pathogenesis is also explored, because they augment keratinocyte responses to proinflammatory cytokines. The discovery of these genetic mutations in familial and pustular psoriasis suggests new links between cytokine-induced gene products and IL-1 family members from keratinocytes, which may regulate features of the disease, including epidermal hyperplasia and neutrophil infiltrating responses.
journal_name
Trends Immunoljournal_title
Trends in immunologyauthors
Lowes MA,Russell CB,Martin DA,Towne JE,Krueger JGdoi
10.1016/j.it.2012.11.005subject
Has Abstractpub_date
2013-04-01 00:00:00pages
174-81issue
4eissn
1471-4906issn
1471-4981pii
S1471-4906(12)00199-8journal_volume
34pub_type
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journal_title：Trends in immunology
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