Abstract
Chemokines are critical for the inflammatory process in autoimmune diseases such as rheumatoid arthritis (RA). The chemokine receptor-5 (CCR5) mediates chemotaxis by CC-chemokines and is expressed by lymphocytes with the Th1 phenotype and monocyte/macrophages. A 32 bp deletion in the CCR5 (CCR5-Δ32 allele) abolishes receptor expression in homozygotes, while CCR5-Δ32 carriers would express less receptor than wild-type homozygotes. This polymorphism is related to the resistance to HIV-1 infection and progression towards AIDS. We hypothesized that the CCR5-Δ32 allele may modulate the severity of disease in RA. A total of 160 RA-patients (71 and 89 with severe and non-severe phenotypes, respectively) and 500 healthy individuals from the same Caucasian population (Asturias, northern Spain) were genotyped. Carriers of the CCR5-Δ32 allele were at a significantly higher frequency (P = 0.012) in non-severe compared to severe patients (17% vs 4%). Our results suggest that the CCR5-Δ32 polymorphism is a genetic marker related to the severity of RA.
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This work was supported in part by a grant from the Spanish Fondo de Investigaciones Sanitarias (Fiss 00/0239) to VA.
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Zapico, I., Coto, E., Rodríguez, A. et al. CCR5 (chemokine receptor-5) DNA-polymorphism influences the severity of rheumatoid arthritis. Genes Immun 1, 288–289 (2000). https://doi.org/10.1038/sj.gene.6363673
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DOI: https://doi.org/10.1038/sj.gene.6363673
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