Document Detail

Current understanding of the genetic basis of psoriasis.
MedLine Citation:
PMID:  20477039     Owner:  NLM     Status:  PubMed-not-MEDLINE    
Psoriasis is a common, immunologically mediated, inflammatory and hyperproliferative disease of the skin and joints, with a multifactorial genetic basis. Recently, the association of psoriasis with loci at HLA-Cw*0602, IL12B, IL23A, IL23R, TNFAIP3, TNIP1, ZNF313 and IL4/IL13, and copy number variations in the beta-defensin and late-cornified envelope (LCE) gene loci were described. Here, we discuss the advances in the technology that has lead to the identification of these genes and their presumed role in the pathogenesis of psoriasis. Although it is now generally accepted that psoriatic lesions are caused by abnormal reactivity of specific T cells in the skin, these findings suggest that alterations in the epidermal barrier, innate defenses and processing of inflammatory signals may all contribute to the triggering of nonspecific innate immune mechanisms, which, in combination with altered IL-23 signaling, may lead to the dysregulation of T-cell-driven immune responses.
Johann E Gudjonsson; Andrew Johnston
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Publication Detail:
Type:  Journal Article    
Journal Detail:
Title:  Expert review of clinical immunology     Volume:  5     ISSN:  1744-8409     ISO Abbreviation:  Expert Rev Clin Immunol     Publication Date:  2009 Jul 
Date Detail:
Created Date:  2010-05-18     Completed Date:  2010-06-18     Revised Date:  -    
Medline Journal Info:
Nlm Unique ID:  101271248     Medline TA:  Expert Rev Clin Immunol     Country:  England    
Other Details:
Languages:  eng     Pagination:  433-43     Citation Subset:  -    
Department of Dermatology, University of Michigan, Room 6427, Medical Science Building I, 1301 Catherine, Ann Arbor, MI, USA.
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