Background and Objectives: CC chemokine receptor type 5 (CCR5) is a chemokine receptor expressed at high levels on the surface of T-cells. A 32-bp deletion in the coding region of the CCR5 (CCR5Î32) leads to production of an incomplete protein that is not expressed on the cell surface. CCR5Î32 may be involved in development of autoimmune disease, such as systemic lupus erythematosus. We investigated frequency of the CCR5Î32 polymorphism in SLE patients and healthy controls, and evaluated the relationship between the CCR5Î32 polymorphism and susceptibility to SLE in Golestan Province, Iran. Methods: Whole blood samples were taken from 80 SLE patients admitted to Shahid Sayyad Shirazi hospital and 80 healthy controls (from a blood bank) in the Golestan Province, in 2016. Baseline clinical and laboratorial characteristics were evaluated regarding the CCR5Î32 genotypes. The CCR5Î32 polymorphism was determined from genomic DNA by polymerase chain reaction. Result: Genotype frequencies of both groups were in the Hardy-Weinberg equilibrium. The frequencies of the CCR5 and the CCR5Î32 alleles were 98.13% and 1.88% among the patients, and 98.75% and 1.25% among the controls, respectively. Homozygote CCR5Î32 was not observed in the subjects. The frequency of heterozygous Î32 was 3.8% and 2.5% among the SLE patients and controls, respectively (P-value>0.05). There was no significant association between the CCR5 status and clinical signs of SLE (P>0.05). Conclusion: Our data suggest that the CCR5Î32 polymorphism has no correlation with SLE in our study population. In addition, the frequency of the Î32 polymorphism in SLE patients and controls does not follow the Hardy-Weinberg equilibrium