title: Association of interleukin-4 gene polymorphisms with ischemic heart failure.
abstract: BACKGROUND
  As of the potential immunomodulatory effects of interleukin-4 (IL-4) and its importance in inhibiting the production of proinflammatory cytokines by monocytes and activated T cells, the IL-4 gene polymorphisms were investigated in a group of patients with chronic heart failure due to ischemic heart disease.
  
  
  METHODS
  Forty three patients with ischemic heart failure (IHF) were enrolled in this study and compared with 139 healthy individuals. The allele and genotype frequency of 3 single nucleotide polymorphisms within the IL-4 gene were determined.
  
  
  RESULTS
  The frequency of the IL-4 -590/T allele in the patient group was significantly higher than in the control group (p < 0.0001). The most frequent genotypes in patients with IHF were IL-4 (-590) CC (p < 0.0001), IL-4 (-33) CC (p = 0.021), and IL-4 (-33) TT (p < 0.0001). The frequency of the following genotypes was significantly lower in patients compared to controls: IL-4 (-1098) TG (p = 0.035), IL-4 (-590) TC (p < 0.0001), and IL-4 (-33) TC (p < 0.0001). The most frequent IL-4 haplotypes in the patient group, which were significantly higher than in the control group, were TCC (p < 0.0001), TCT (p = 0.0242), and GCT (p = 0.0108) haplotypes. In contrast, the frequencies of the following haplotypes in the patient group were significantly lower than in the controls: GCC (p = 0.032), TTT (p = 0.0268), and TTC (p = 0.0399).
  
  
  CONCLUSIONS
  Certain alleles, genotypes, and haplotypes in IL-4 gene were over represented inpatients with IHF, which may, in turn, predispose individuals to this disease.
authors.forename: Mohammad Jafar
authors.initials: MJ
authors.lastname: Mahmoudi
authors.forename: Mona
authors.initials: M
authors.lastname: Hedayat
authors.forename: Mohammad
authors.initials: M
authors.lastname: Taghvaei
authors.forename: Ebrahim
authors.initials: E
authors.lastname: Nematipour
authors.forename: Elham
authors.initials: E
authors.lastname: Farhadi
authors.forename: Nilufar
authors.initials: N
authors.lastname: Esfahanian
authors.forename: Maryam
authors.initials: M
authors.lastname: Sadr
authors.forename: Maryam
authors.initials: M
authors.lastname: Mahmoudi
authors.forename: Keramat
authors.initials: K
authors.lastname: Nourijelyani
authors.forename: Ali Akbar
authors.initials: AA
authors.lastname: Amirzargar
authors.affiliation: Molecular Immunology Research Center, Tehran University of Medical Sciences, Tehran, Iran; Department of Immunology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran; Research Center for Immunodeficiencies, Children's Medical Center, Tehran University of Medical Sciences, Tehran, Iran. rezaei_nima@tums.ac.ir.
authors.forename: Nima
authors.initials: N
authors.lastname: Rezaei
mesh_terms: D004247:DNA / Q000235:genetics*; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006239:Haplotypes; D006333:Heart Failure / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D006801:Humans; D015847:Interleukin-4 / Q000235:genetics* / Q000378:metabolism; D008297:Male; D008875:Middle Aged; D017202:Myocardial Ischemia / Q000150:complications / Q000235:genetics* / Q000378:metabolism; D016133:Polymerase Chain Reaction; D011110:Polymorphism, Genetic
chemical_list: C508598:IL4 protein, human; D015847:Interleukin-4; D004247:DNA