The contribution ofpolymorphism of DMA and DMB alleles to the pathogenesis of Japanese RA was studied.
The association of DM alleles with HLA-DRB1*0405 and *0802, which were positively and negatively susceptible to Japanese RA, respectively, is also discussed.
DMA and DMB typing was carried out in 91 Japanese RA patients and in 77 normal subjects by the PCR-RFLP (restriction fragment length polymorphism) method.
HLA-DRB1*04 and *08 genotyping were carried out by the PCR-SSCP (single-stranded DNA conformation polymorphism) method.
Allele frequencies of DMB*0101 and DMB*0102 were slightly higher (52.2% and 27.0%) and the allele frequency of DMB*0103 was slightly lower (25.8%) in RA, but these differences were not significant.
The increase of DMB*0102 was due to a negative association with HLA-DRB1*0802 [p<0.05, pc=not significant (NS) ]. The decrease Of DMB*0103 was due to a positive association with DRBI*0802 (p<0.005, pc<0.05).
The increase of DMB*0101 was possibly due to a weak association with HLA-DRB1*0405, (p=NS).
Positivity of rheumatoid factor did not affect the prevalence of DMA and DMB alleles.
Association analysis among DMA, DMB and DRBI (*0405 and *0802) indicate that slight increases or decreases in DMB*0101, DMB*0102 and DMB*0103 are not primary indicators but reflect an increase in HLA-DRB1* 0405 and a decrease in HLA-DRB1*0802 in Japanese RA.
Mots-clés Pascal : Polyarthrite rhumatoïde, Homme, Pathogénie, Déterminisme génétique, Système HLA, Antigène histocompatibilité classe II, Epidémiologie, Japonais, Prévalence, Réaction chaîne polymérase, Polymorphisme longueur fragment restriction, Génotype, Allèle, Phénotype, Chronique, Système ostéoarticulaire pathologie, Rhumatisme inflammatoire, Immunopathologie, Maladie autoimmune, Biologie moléculaire
Mots-clés Pascal anglais : Rheumatoid arthritis, Human, Pathogenesis, Genetic inheritance, HLA-System, Class II histocompatibility antigen, Epidemiology, Japanese, Prevalence, Polymerase chain reaction, Restriction fragment length polymorphism, Genotype, Allele, Phenotype, Chronic, Diseases of the osteoarticular system, Inflammatory joint disease, Immunopathology, Autoimmune disease, Molecular biology
Notice produite par :
Inist-CNRS - Institut de l'Information Scientifique et Technique
Cote : 97-0319957
Code Inist : 002B15D. Création : 12/09/1997.