CCR5 (chemokine receptor-5) DNA-polymorphism influences the severity of rheumatoid arthritis.
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-delta 32 allele) abolishes receptor expression in homozygotes, while CCR5-delta 32 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-delta 32 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-delta 32 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-delta 32 polymorphism is a genetic marker related to the severity of RA.
Zapico
I
I
Servicio de Reumatología, Hospital Central de Asturias, Oviedo, Spain.
Coto
E
E
Rodríguez
A
A
Alvarez
C
C
Torre
J C
JC
Alvarez
V
V
D001172:Arthritis, Rheumatoid / Q000235:genetics* / Q000378:metabolism; D018925:Chemokines / Q000378:metabolism; D005260:Female; D020022:Genetic Predisposition to Disease; D006801:Humans; D008297:Male; D008875:Middle Aged; D011110:Polymorphism, Genetic; D019713:Receptors, CCR5 / Q000235:genetics* / Q000378:metabolism; D012720:Severity of Illness Index
D018925:Chemokines; D019713:Receptors, CCR5