title: [Interleukin-1 and the interleukin-1 receptor antagonist gene polymorphisms study in patients with rheumatoid arthritis].
abstract: OBJECTIVE
  One of the most important pro-inflammatory cytokines in the pathophysiology of rheumatoid arthritis (RA) is interleukin 1 (IL-1). The purpose of this study is to evaluate the association between IL-1B (-511), IL-1 (+3953), IL-1 RN variable number of tandem repeat (VNTR) polymorphisms and the occurrence in Algerian patients with rheumatoid arthritis. We also analyze their correlations with clinical and biological phenotypes.
  
  
  METHODS
  One hundred and forty-seven patients with RA (119 women, 28 men) and 127 controls (70 women, 57 men) were included in the study. The analysis of two polymorphisms of IL-1B-511 and IL-1B+3953 was done by PCR-RFLP. Analysis of IL1-RN VNTR polymorphism was performed by PCR.
  
  
  RESULTS
  No significant difference in genotype, allelic and haplotype distribution at the three polymorphisms was observed between RA patients and controls. However, the genotype (T/T) polymorphism of IL-1B-511 is more frequent in the group of patients with positive ACPA compared with negative ACPA group (Pc=0.01, OR=4.65). Moreover, we noted that the haplotype (IL-1RN* 1/IL-1B-511T/IL-1B+3953C) was more frequent (Pc=0.03, OR=2.05) in the positive ACPA group.
  
  
  CONCLUSIONS
  The association between the allele 1 of IL-1 RN VNTR, T allele of IL1B-511 and C allele of IL1-B +3953 polymorphisms seems to predispose to the synthesis of ACPA and therefore to the occurrence of ACPA positive RA. Further studies with a larger number of patients are needed to define the real role of IL-1 in the susceptibility to or severity of RA.
authors.affiliation: Unité d'immunologie, laboratoire de biologie médicale, centre hospitalier universitaire Béni-Messous, Alger, Algérie.
authors.forename: I
authors.initials: I
authors.lastname: Allam
authors.forename: R
authors.initials: R
authors.lastname: Djidjik
authors.forename: N
authors.initials: N
authors.lastname: Ouikhlef
authors.forename: S
authors.initials: S
authors.lastname: Louahchi
authors.forename: N
authors.initials: N
authors.lastname: Raaf
authors.forename: N
authors.initials: N
authors.lastname: Behaz
authors.forename: A
authors.initials: A
authors.lastname: Abdessemed
authors.forename: N
authors.initials: N
authors.lastname: Khaldoun
authors.forename: A
authors.initials: A
authors.lastname: Tahiat
authors.forename: M
authors.initials: M
authors.lastname: Bayou
authors.forename: A
authors.initials: A
authors.lastname: Ladjouze-Rezig
authors.forename: M
authors.initials: M
authors.lastname: Ghaffor
mesh_terms: D000328:Adult; D001172:Arthritis, Rheumatoid / Q000097:blood / Q000235:genetics*; D001323:Autoantibodies / Q000097:blood; D016022:Case-Control Studies; D002956:Citrulline / Q000276:immunology / Q000378:metabolism; D005260:Female; D005787:Gene Frequency; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006801:Humans; D053590:Interleukin 1 Receptor Antagonist Protein / Q000235:genetics*; D053583:Interleukin-1beta / Q000235:genetics*; D008297:Male; D008875:Middle Aged; D018598:Minisatellite Repeats / Q000235:genetics; D010446:Peptide Fragments / Q000276:immunology / Q000378:metabolism; D011110:Polymorphism, Genetic
chemical_list: D001323:Autoantibodies; D053590:Interleukin 1 Receptor Antagonist Protein; D053583:Interleukin-1beta; D010446:Peptide Fragments; D002956:Citrulline
keywords: Anti-citrullinated protein autoantibody; Anticorps anti-peptides citrullinés; IL-1; IL1-RN; Polyarthrite rhumatoïde; Polymorphism; Polymorphisme; Rheumatoid arthritis