Endothelial dysfunction and inflammation are involved in the pathogenesis of preeclampsia. The CC chemokine receptor 5 (CCR5) modulates inflammation secondary to endothelial dysfunction and related vascular disorders, by initiating chemotaxis. In this study, we examined the frequency of two polymorphisms, the CCR5D32 deletion and the CCR5-59029 A/G promoter point mutation in women with preeclampsia. The CCR5 polymorphisms were genotyped in 74 preeclamptic and 128 controls who had been unaffected by preeclampsia in previous pregnancies. Genotyping was performed with the polymerase chain reaction and restriction fragment length polymorphism. Statistical evaluations were made using the chi-square test or Fisher's exact test when appropriate. The percentage of wild-type allele bearers (?/?plus ?/D32 genotypes) in the preeclamptic group was significantly higher than that of non-bearers (98.6 vs.91.4%, P = 0.03, by the Fisher's exact test). The number of the individuals with D32/D32 genotype was significantly high in the control group (P = 0.035). D32 allele revealed a 2.3-fold protective effect against the risk of preeclampsia.When the percentage of G allele bearers of CCR5 59029A/G polymorphism was compared between the groups, a significant increase was seen in preeclamptics (P = 0.002). CCR5 polymorphisms significantly influenced the susceptibility to preeclampsia in our study population consisted of Caucasians. The role of chemokines in this syndrome appears to be an important issue.