title: The A/A genotype of an interleukin-17A polymorphism predisposes to increased severity of atopic dermatitis and coexistence with asthma.
abstract: BACKGROUND
  Studies have found that the interleukin-23/T helper 17 (IL-23/Th17) pathway plays an important role in the pathogenesis of atopic dermatitis (AD). Inhibition of the IL-23/Th17 pathway with monoclonal antibodies reduces skin inflammation in animal models.
  
  
  OBJECTIVE
  To investigate the association between IL-17A and IL-23R gene single nucleotide polymorphisms (SNPs) and the development of AD in a Polish population.
  
  
  METHODS
  Blood samples were collected from 166 patients with AD and 160 controls. We analyzed two SNPs, -152 G/A IL-17A and 1142 G/A IL-23R, using PCR and restriction fragment length polymorphism (RFLP) analysis.
  
  
  RESULTS
  There was no statistically significant difference between the examined IL-17A SNP and the incidence of AD (P > 0.05 for all comparisons). Analysis of the IL-23R gene SNP showed no relationship between AD and the G/A genotype or presence of the A allele. The study did not establish any links between the IL-23R and IL-17A gene SNPs and the likelihood of developing AD resulting from gene-gene interaction. However, there was a significant relationship between the A/A genotype in the -152 G/A IL1-7A SNP and the coexistence of AD and asthma (P < 0.04). Analyzing the association between AD severity and the occurrence of IL-17A SNP, we found that subjects with the A/A genotype were at higher risk of developing moderate or severe AD (P = 0.02).
  
  
  CONCLUSIONS
  We found no evidence of any effect of IL-17A or IL-23R SNPs on the occurrence of AD in our Polish population. However, the A/A genotype in IL-17A was found to predispose to increased AD severity and coexistence of AD and asthma.
authors.affiliation: Department of Dermatology and Venereology, Medical University of Lodz, Lodz, Poland.
authors.forename: J
authors.initials: J
authors.lastname: Narbutt
authors.forename: M
authors.initials: M
authors.lastname: Wojtczak
authors.forename: A
authors.initials: A
authors.lastname: Zalińska
authors.forename: A
authors.initials: A
authors.lastname: Salinski
authors.forename: K
authors.initials: K
authors.lastname: Przybylowska-Sygut
authors.forename: P
authors.initials: P
authors.lastname: Kuna
authors.forename: P
authors.initials: P
authors.lastname: Majak
authors.forename: A
authors.initials: A
authors.lastname: Sysa-Jedrzejowska
authors.forename: A
authors.initials: A
authors.lastname: Lesiak
mesh_terms: D000293:Adolescent; D000328:Adult; D000483:Alleles; D001249:Asthma / Q000150:complications*; D016022:Case-Control Studies; D002648:Child; D002675:Child, Preschool; D003876:Dermatitis, Atopic / Q000150:complications / Q000453:epidemiology / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D015994:Incidence; D007223:Infant; D020381:Interleukin-17 / Q000235:genetics*; D008297:Male; D011044:Poland / Q000453:epidemiology; D012150:Polymorphism, Restriction Fragment Length; D020641:Polymorphism, Single Nucleotide; D018123:Receptors, Interleukin / Q000235:genetics; D012720:Severity of Illness Index; D055815:Young Adult
chemical_list: C515500:IL23R protein, human; D020381:Interleukin-17; D018123:Receptors, Interleukin