English (United Kingdom)

https://curated-unify.zendy.io/wp-json/zendy-region/v1/featured_content/oa?rat=en

https://curated-unify.zendy.io/wp-json/zendy-region/v1/highlighted_journal/

Global: Zendy Plus annual

Presents the access of premium content as premium feature

Premium Content

Presents the keyphrase highlighting as premium feature

Keyphrase Highlighting

Presents the summarisation as premium feature

Summarisation

Insights

Presents the pdf analysis as premium feature

PDF Analysis

Presents the zaia usage as premium feature

ZAIA

Global: Zendy Tools annual

Global: Zendy Free Plan

Global: Zendy Tools monthly

Global: Zendy Plus monthly

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].

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