The toll-like receptor 2 R753Q polymorphism defines a subgroup of patients with atopic dermatitis having severe phenotype.

Journal of Allergy and Clinical Immunology (Impact Factor: 11.25). 04/2004; 113(3):565-7. DOI: 10.1016/j.jaci.2003.12.583
Source: PubMed
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    ABSTRACT: Atopic dermatitis is a common chronic inflammatory skin disease and depends on the interaction between environmental factors and genetic predisposition. A considerable role in allergic disorders is played by polymorphisms of the genes of pattern recognition receptors (PRRs), which recognize conserved standard molecular structures (patterns) unique to large pathogen groups. Polymorphisms of several PRR genes, including the genes of Toll-like receptors (TLR1, TLR2, TLR4, TLR5, TLR6, TLR9, and TLR10), NOD-like receptors (NOD1 and NOD2), and a lipopolysaccharide receptor (CD14) along with C11orf30 and LRRC32 from chromosome 11q13.5, were studied in atopic dermatitis patients and control subjects from Bashkortostan. TLR1 (rs5743571 and rs5743604), TLR6 (rs5743794), and TLR10 (rs11466617) polymorphisms were associated with atopic dermatitis. The results supported the idea that innate immunity and polymorphisms of the TLR2-family genes play a substantial role in atopic dermatitis.
    Molecular Biology 03/2014; 48(2):227-237. DOI:10.1134/S002689331402006X · 0.74 Impact Factor
  • New England Journal of Medicine 04/2008; 358(14):1483-94. DOI:10.1056/NEJMra074081 · 54.42 Impact Factor
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    ABSTRACT: Part 3 of this three-part review of atopic dermatitis and the stratum corneum barrier discerns how immune dysregulation, including upregulation of a TH2 inflammation pattern, augmented allergic sensitization, sustained wound healing inflammation, and impaired innate immunity, plays an integral role in the pathogenesis of atopic dermatitis. An increased understanding of the interdependence, polymorphisms, and dysregulations of epidermal barrier functions, including the stratum corneum permeability barrier, immune defense, and antimicrobial barriers, should provide further knowledge about the pathophysiological mechanisms that are clinically relevant and that contribute to the development of atopic dermatitis. Further understanding of these mechanisms should lead to newer therapies that target specific pathogenic components of atopic dermatitis.
    Journal of Clinical and Aesthetic Dermatology 12/2013; 6(12):37-44.