Rheumatoid arthritis is an inflammatory disease driven by TH1 CD4+ cells. Interleukin-10 is present in higher concentrations in serum and synovial fluid from patients with rheumatoid arthritis and has a marked anti-inflammatory activity. Furthermore, it is capable of stimulating B cells and increasing autoantibody production. Interleukin-10 synthesis is under genetic control.
Three polymorphisms of the promoter region were analyzed for interleukin-10 genes -1082, -819 and -592. Subjects were patients with rheumatoid arthritis compared with a control population for these genes.
One hundred two patients with rheumatoid arthritis and 102 matched healthy controls were studied. The following data were taken from the rheumatoid arthritis patients: age of disease onset, presence and titers of rheumatoid factor, and history of replacement joint surgery. Genotypes were obtained by polymerase chain reaction and sequence-specific primer method. The three polymorphisms are in strong linkage-disequilibrium and form three haplotypes -1082A/-819C/-592C, -1082A/-819T/-592A y -1082G/-819C/-592C.
No association was detected between Interleukin-10 alleles, haplotypes/genotypes and rheumatoid arthritis. No significant differences occurred between interleukin-10 polymorphisms and age of disease onset, presence and titer of rheumatoid factor and history of major joint replacement.
Interleukin-10 is an important regulator of the immune response and likely plays a role in the pathogenesis of rheumatoid arthritis. The current results suggested that Interleukin-10 promoter polymorphisms were not important for development or severity of rheumatoid arthritis.