Ichthyosis vulgaris is caused by loss-of-function mutations in the filaggrin gene (FLG) and is characterized clinically by xerosis, scaling, keratosis pilaris, palmar and plantar hyperlinearity, and a strong association with atopic disorders.
To determine whether filaggrin (FLG) variants can serve as a predictor for atopic disorders in Chinese individuals and if allergen exposures may modify the effect of FLG variants on AD by total IgE levels.
Loss of function FLG alleles were first identified as causative of ichthyosis vulgaris (IV) and were subsequently found to be major predisposing factors for atopic dermatitis (AD) and atopic disorders.
Genetic association studies of the CD14 gene with asthma and atopic disorders have shown positive as well as negative results in different ethnic populations.
We studied a cohort containing 368 children at high risk of developing atopy and atopic disorders and 540 parents of those children to investigate whether the IL13Arg130Gln and C-1112 T polymorphisms were associated with these outcomes.
These studies validate the genetic hypothesis that the TIM-1 locus is linked to the development of atopic disease and suggest novel therapeutic strategies for targeting asthma and other atopic disorders.
We also noted genes associated with autoimmune and atopic disorders.<b>Conclusions:</b> Findings from this study suggest that genetic variants in immune pathways are relevant to breast cancer susceptibility among AA women, both for ER<sup>+</sup> and ER<sup>-</sup> breast cancers.<b>Impact:</b> Results from this study extend our understanding of how inherited genetic variation in immune pathways is relevant to breast cancer susceptibility.
These studies validate the genetic hypothesis that the TIM-1 locus is linked to the development of atopic disease and suggest novel therapeutic strategies for targeting asthma and other atopic disorders.
We aimed to identify variants of MCC and another gene within this complex, and assess whether there is a genetic association between variants of MCC and atopic disorders-particularly eczema.
These results do not confirm previous case-control studies and suggest that IL15 gene variants do not play an important role in the development for asthma or other atopic disorders.
In our cohort, the proportion of males to females with CHARGE and atopic disorders was 11:4 (P < 0.01), and there was no significant difference between atopic disorders in individuals with CHD7 pathogenic variants and those without CHD7 pathogenic variants (P > 0.05).
Polymorphisms in N-acetyltransferase 2 (NAT2), present on chromosome 8p22, are responsible for the N-acetylation variants, which segregate human populations into rapid, intermediate and slow acetylators and influence the susceptibility towards atopic disorders.
Genetic variants of CARD15 that might result in inappropriate immunomodulation are not only associated with autoimmune diseases but also with atopic disorders.
These studies validate the genetic hypothesis that the TIM-1 locus is linked to the development of atopic disease and suggest novel therapeutic strategies for targeting asthma and other atopic disorders.
IL-4 plays a pivotal role in the development of allergic inflammation via induction of IgE isotype switching, increase of IgE receptor expression, promoting Th2 cell differentiation, and stimulating several genes involved in atopic disorders.
We report here the identification of 26 single-nucleotide polymorphisms (SNPs) spanning a total of 147 kb in two candidate genes, IL4RA and STAT6, for atopic disorders.