title: Association of the HLA-G 14-bp insertion/deletion polymorphism with juvenile idiopathic arthritis and rheumatoid arthritis.
abstract: We tested the possible association of the 14-bp polymorphism of the HLA-G gene in the course of two inflammatory diseases, rheumatoid arthritis (RA) and juvenile idiopathic arthritis (JIA). Patients and controls were genotyped for the 14-bp polymorphism by polymerase chain reaction with specific primers for the exon 8 of the human leukocyte antigen (HLA)-G gene and the amplified fragment was visualized in a 6% polyacrylamide gel. A total of 106 JIA patients, 265 RA patients, 356 healthy adults and 85 healthy children were genotyped for the 14-bp polymorphism. Female JIA patients presented a higher frequency of the -14 bp allele when compared with female healthy children (0.743 and 0.500, corrected P=0.003), which reflected in the JIA group as a whole. This increased frequency of the -14-bp allele was observed in all JIA subtypes. In RA patients, no differences in allelic and genotypic frequencies were observed between patients and controls. No correlations were observed among genotype and disease severity or clinical manifestations. Our data suggest that the HLA-G -14 bp allele is probably a risk factor for JIA, mainly in females. Considering the differences observed in relation to gender, we suggest that hormonal differences can interfere with the development of JIA. Considering the RA patients, our data agree with results from the literature and highlight the differences in the etiology of RA and JIA.
authors.affiliation: Genetics Department, Universidade Federal do Rio Grande do Sul, Porto Alegre, Brazil.
authors.forename: Tiago Degani
authors.initials: TD
authors.lastname: Veit
authors.forename: Priscilla
authors.initials: P
authors.lastname: Vianna
authors.forename: Ilóite
authors.initials: I
authors.lastname: Scheibel
authors.forename: Claiton Viegas
authors.initials: CV
authors.lastname: Brenol
authors.forename: Claiton
authors.initials: C
authors.lastname: Brenol
authors.forename: João Carlos Tavares
authors.initials: JC
authors.lastname: Brenol
authors.forename: Ricardo Machado
authors.initials: RM
authors.lastname: Xavier
authors.forename: Andres
authors.initials: A
authors.lastname: Delgado-Cañedo
authors.forename: Jorge Eduardo
authors.initials: JE
authors.lastname: Gutierrez
authors.forename: Ana Paula Carneiro
authors.initials: AP
authors.lastname: Brandalize
authors.forename: Lavinia
authors.initials: L
authors.lastname: Schuler-Faccini
authors.forename: José Artur Bogo
authors.initials: JA
authors.lastname: Chies
mesh_terms: D000293:Adolescent; D000368:Aged; D000483:Alleles; D001171:Arthritis, Juvenile / Q000235:genetics*; D001172:Arthritis, Rheumatoid / Q000235:genetics*; D002648:Child; D002675:Child, Preschool; D005260:Female; D020022:Genetic Predisposition to Disease; D005838:Genotype; D006680:HLA Antigens / Q000235:genetics*; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I / Q000235:genetics*; D006801:Humans; D008297:Male; D008875:Middle Aged; D016254:Mutagenesis, Insertional; D011110:Polymorphism, Genetic; D017384:Sequence Deletion
chemical_list: D006680:HLA Antigens; D059951:HLA-G Antigens; D015395:Histocompatibility Antigens Class I