Considerations About the Role of the CCR5 Gene in Juvenile Idiopathic Arthritis - Look at the Whole or Put All Parts Together?

The CCR5 is an important chemockine receptor. The gene coding for this protein initially gain attention when a variant called CCR5 32 (due to the occurrence of a 32 base pair deletion in its coding region) was associated to resistance against HIV infection. Thus, homozigous CCR5 32 individuals were shown to be protected against HIV-1 infection and heterozigous individuals presented a delay on AIDS development [1, 2]. From this sparkling start, the CCR5 gene, and specifically the CCR5 32 allele, become a candidate and a target to several studies intending to understand and explore such “beneficial allelic variant”. In this way, in 1998 the CCR5 32 variant was suggested to act as a protective factor against the development of rheumatoid arthritis (RA) [3] and since then several works were published attempting to corroborate or refute this initial idea and also attempting to inhibit this chemokine receptor, as a therapeutic approach in order to modulate rheumatoid arthitis symptons [4-9].