Journal
JOURNAL OF INVESTIGATIVE DERMATOLOGY
Volume 130, Issue 8, Pages 2057-2061Publisher
ELSEVIER SCIENCE INC
DOI: 10.1038/jid.2010.88
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Funding
- German Ministry of Education and Research (BMBF), National Genome Research Network (NGFN) [01GS0818]
- University Hospital Rechts der Isar, Technische Universitat Munchen [C49-08]
- Wilhelm-Vaillant-Stiftung
- German Research Council [DFG WE 2678/4-1, NO454/5-2, SFB704 TPA4]
- Children's Medical and Research Foundation
- MRC [G0700314] Funding Source: UKRI
- Medical Research Council [G0700314] Funding Source: researchfish
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Atopic dermatitis (AD) and psoriasis are common skin diseases characterized by cutaneous inflammation and disturbed epidermal differentiation. Genome-wide analyses have shown overlapping susceptibility loci, such as the epidermal differentiation complex on chromosome 1q21. Recently, a deletion on 1q21 (LCE3C_LCE3B-del), comprising LCE3B and LCE3C, two members of the late cornified envelope (LCE) gene cluster, was found to be associated with psoriasis. Although the mechanistic role of LCE proteins in psoriasis has not been identified, these proteins are putatively involved in skin barrier formation and repair. Considering the potential genetic overlap between the two diseases and the recent finding that mutations in the skin barrier protein filaggrin are associated with AD, we investigated a possible association between LCE3C_LCE3B-del and AD. Evaluation of four different cohorts of European ancestry, containing a total of 1075 AD patients and 1658 controls, did not provide evidence for such an association. Subgroup analysis did not reveal an association with concomitant asthma. Our data suggest that the potential roles of skin barrier defects in the pathogenesis of AD and psoriasis are based on distinct genetic causes.
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