Rheumatoid arthritis (RA) is an inflammatory joint disorder whose progression leads to destruction of cartilage and bone.
Chemokines, molecules able to induce chemotaxis in inflammation, are involved in RA pathogenesis. Aim of this study
was to determine whether -2150 A>G and delta32 (Δ32) polymorphisms in the chemokine receptor 5 (CCR5) confer
susceptibility to rheumatoid arthritis. Polymorphisms were assessed in 70 seropositive RA patients and 200 healthy
individuals of Messina and province. About -2150 A>G polymorphism, a significant increase in AG genotype frequency
was observed in controls than in patients, despite a not significant difference in allelic frequencies. Conversely,
allelic and genotypic frequencies related to Δ32 polymorphism were significantly higher in controls group than
in patients. Furthermore, in the patient group no individuals with Δ32/Δ32 genotype were found. These results
suggest that CCR5 polymorphisms seem to play an important role in susceptibility to RA exerting a protective role
in the disease.