title: Interleukin 13 receptors as biochemical markers in atopic patients.
abstract: BACKGROUND
  Interleukin (IL) 13, a type 2 helper T cell (T(H)2), is an important regulator of inflammatory immune responses. It mediates its action through a receptor complex consisting of IL-13Ralpha1 and IL-4Ralpha. IL-13Ralpha2 binds IL-13 with high affinity and is thought to act primarily as a decoy receptor, sequestering IL-13 and thus inhibiting its action. Our aim was to clarify the role of these receptors in the diagnosis and follow-up of atopic patients.
  
  
  METHODS
  We genotyped the 1398A>G polymorphism in the IL-13Ralpha1 gene using restriction fragment length polymorphism for causal genetic diversity and measured serum levels of IL-13Ralpha2 in 105 atopic patients suffering from atopic asthma, atopic dermatitis, and atopic rhinitis (35 each). We compared the results with those of 35 nonatopic control individuals. Total immunoglobulin (Ig) E and serum IL-13Ralpha2 were measured using enzyme-linked immunosorbent assay, and the eosinophil counts were recorded.
  
  
  RESULTS
  A significant increase in serum IL-13Ralpha2 levels was recorded in the 3 atopic groups compared with the control group (P < .001), as well as a significant increase in total IgE levels and eosinophil counts. No significant association was found between 1398A>G and atopy other than a suggestive association between this polymorphism and raised total serum IgE levels in all 3 atopic groups (P < .001).
  
  
  CONCLUSIONS
  These findings indicate that IL-13Ralpha2 plays an important role in atopy and that increased levels in different groups highlight its regulatory role in the development of atopic symptoms. The 1398A>G polymorphism might be involved in the production of IgE.
authors.affiliation: Medical Biochemistry Department, Faculty of Medicine, Zagazig University, Egypt. yousrihussein@hotmail.com
authors.forename: Y M
authors.initials: YM
authors.lastname: Hussein
authors.forename: A S
authors.initials: AS
authors.lastname: Ahmad
authors.forename: M M
authors.initials: MM
authors.lastname: Ibrahem
authors.forename: H M
authors.initials: HM
authors.lastname: Elsherbeny
authors.forename: S M
authors.initials: SM
authors.lastname: Shalaby
authors.forename: A S
authors.initials: AS
authors.lastname: El-Shal
authors.forename: N A
authors.initials: NA
authors.lastname: Sabbah
mesh_terms: D001249:Asthma / Q000097:blood / Q000235:genetics / Q000276:immunology; D015415:Biomarkers / Q000032:analysis*; D016022:Case-Control Studies; D003876:Dermatitis, Atopic / Q000097:blood / Q000235:genetics / Q000276:immunology; D004804:Eosinophils / Q000166:cytology; D005260:Female; D005838:Genotype; D006801:Humans; D007073:Immunoglobulin E / Q000097:blood; D007958:Leukocyte Count; D011110:Polymorphism, Genetic; D053660:Receptors, Interleukin-13 / Q000097:blood / Q000235:genetics* / Q000276:immunology*; D012220:Rhinitis / Q000097:blood / Q000235:genetics / Q000276:immunology
chemical_list: D015415:Biomarkers; D053660:Receptors, Interleukin-13; D007073:Immunoglobulin E