Psoriasis Research Today is a free monthly online journal that collates and summarizes the latest research about Psoriasis, including details on treatment, prevention, medication, causes.

Filaggrin null alleles are not associated with psoriasis.

Zhao Y, Terron-Kwiatkowski A, Liao H, Lee SP, Allen MH, Hull PR, Campbell LE, Trembath RC, Capon F, Griffiths CE, Burden D, McManus R, Hughes R, Kirby B, Rogers SF, Fitzgerald O, Kane D, Barker JN, Palmer CN, Irvine AD, McLean WH

Epithelial Genetics Group, Human Genetics Unit, Division of Pathology and Neuroscience, University of Dundee, Ninewells Hospital and Medical School, Dundee, UK.

Psoriasis is a common skin disease with an etiology consistent with a multifactorial trait. Several psoriasis susceptibility loci are known, a number of which are also implicated in a predisposition to atopic dermatitis (AD), including the epidermal differentiation complex on chromosome 1q21. It has recently been shown in several replicate studies that prevalent null alleles for the filaggrin gene (FLG) on 1q21 are an important genetic factor in AD. Here, we examined the role of these FLG variants in psoriasis using case:control association studies comparing Irish and UK psoriasis cohorts (combined n=691) to ethnically matched populations (combined n=2117). No association was present for the two common European FLG mutations R501X and 2282del4 (combined chi2 P=0.989). In addition, the 3' end of the FLG open-reading frame was sequenced in a number of patients with differing types of psoriasis (plaque, guttate, palmoplantar, and late-onset), which excluded the possibility of a gain-of-function frameshift mutation such as those found in loricrin or certain keratin genes. These data suggest that FLG mutations are unlikely to be involved in genetic susceptibility to psoriasis and implies that there may be within-locus heterogeneity in chromosomal regions involved in both AD and psoriasis.

Published 16 July 2007 in J Invest Dermatol, 127(8): 1878-82.
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