Interleukin-1 gene polymorphisms in axial spondyloarthritis Tunisian patients.
Adult
Aged
Alleles
Case-Control Studies
Cross-Sectional Studies
Female
Genetic Predisposition to Disease
Genotype
Humans
Interleukin 1 Receptor Antagonist Protein
/ genetics
Interleukin-1
/ genetics
Interleukin-1alpha
/ genetics
Interleukin-1beta
/ genetics
Male
Middle Aged
Polymorphism, Single Nucleotide
Spondylarthritis
/ genetics
Tunisia
Young Adult
Journal
La Tunisie medicale
ISSN: 2724-7031
Titre abrégé: Tunis Med
Pays: Tunisia
ID NLM: 0413766
Informations de publication
Date de publication:
Dec 2020
Dec 2020
Historique:
entrez:
22
1
2021
pubmed:
23
1
2021
medline:
12
10
2021
Statut:
ppublish
Résumé
Axial spondyloarthritis (SpA) is a common inflammatory arthritis characterized by axial skeletal inflammation, enthesitis, and association with HLA-B27. Pro-inflammatory cytokines play important roles in the regulation of inflammatory response and seem to be good candidates involved in the development of this pathology. To assess the influence of the functional polymorphisms of single nucleotide polymorphims (SNPs) of IL-1 and IL-1 Ra in SpA susceptibility Tunisian patients. One hundred and one patients and 100 ethnic-matched healthy controls were genotyped. Susceptibility to SpA was showed with SNP's: C/T of IL-1α (-889) (p=0.0001) and 1/1 of IL-1Ra (p<10-3). Analysis of SpA patients according to clinical behavior of the disease reveled the influence of these polymorphisms in SpA course. Indeed, individuals carrying the allele T (+3954) of IL-1β and allele 1 of IL-1Ra had an increased risk of peripheral arthritis (p=0.047, p=0.05, respectively). Also the 1/1 genotype of IL-1Ra was significantly decreased in SpA patients having an active disease (BASDAI>4) (p=0.033). Genetic polymorphisms of pro-inflammatory IL-1/IL-1Ra cytokines seem to be involved in susceptibility and clinical course of SpA in Tunisian patients.
Substances chimiques
IL1A protein, human
0
IL1B protein, human
0
IL1RN protein, human
0
Interleukin 1 Receptor Antagonist Protein
0
Interleukin-1
0
Interleukin-1alpha
0
Interleukin-1beta
0
Types de publication
Journal Article
Langues
eng
Sous-ensembles de citation
IM