New Insights in the Immunologic Basis of Psoriasis

Kristine E. Nograles, Batya Davidovici, James G. Krueger*

*Corresponding author for this work

Research output: Contribution to journalReview articlepeer-review

Abstract

Psoriasis vulgaris is a multifactorial heritable disease characterized by severe inflammation resulting in poorly differentiated, hyperproliferative keratinocytes. Recent advances in genetic analyses have implicated components regulating the interleukin (IL)-23 and nuclear factor-κB pathways as risk factors for psoriasis. These inflammatory pathways exhibit increased activity in skin lesions, and promote secretion of various cytokines, such as IL-17 and IL-22. Unrestrained, the activated inflammatory cytokine network in psoriasis may trigger a vicious cycle of inflammation and cellular proliferation that ultimately results in lesion formation. These advances in genetic analyses, together with the progress made in targeted biological therapy, pave the path to tailor treatment on the basis of an individual's genetic and immunologic profile.

Original languageEnglish
Pages (from-to)3-9
Number of pages7
JournalSeminars in Cutaneous Medicine and Surgery
Volume29
Issue number1
DOIs
StatePublished - Mar 2010
Externally publishedYes

Funding

FundersFunder number
National Center for Research ResourcesUL1RR024143

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