[Polymorphisms of IL-10 gene promoter and rheumatoid arthritis in a Colombian population].

INTRODUCTION

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.

OBJECTIVE

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.

MATERIAL AND METHODS

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.

RESULTS

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.

CONCLUSIONS

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.