Objective:To explore the expression of C-C chemokine receptor 5（CCR5） in rheumatoid arthritis（RA） by bioinformatic and experimental approaches

to verify the genetic and histological evidence for the involve-ment of CCR5 in the development and progression of RA

and to provide a basis for the follow-up study of the mech-anism of action of CCR5 using a rat model of RA. Methods:The gene chips GSE 97779

GSE 77298

GSE 10500

GSE 55457

and GSE 1919 of RA were searched for in the Gene Expression Omnibus database using rheumatoid ar-thritis as a keyword. Differentially expressed genes were screened for using the bioinformatics analysis tools

GEO2 R and limma

to understand CCR5 expression. The abnormal expression of CCR5 in RA rats was evaluated byimmunohistochemistry

q RT-PCR

and Western blot. Results:In the GSE 1919

GSE 97779

GSE 77298

GSE10500

and GSE 55457 chips

CCR5 expression was abnormally high in RA patients. Moreover

CCR5 was the on-ly gene that was differentially expressed on the five chips. At 10 days after injection of Freund’s complete adjuvant

the rats in the RA group had a substantially increased arthritis index（AI）

which gradually increased with time; AI was significantly higher at 25 days than at 10 and 15 days（7.12 ± 1.13 vs 1.21 ± 0.73 vs 4.87 ± 1.21

P < 0.05）. Theresult of HE staining showed neovascularization and inflammatory cell infiltration in the synovial tissue of the RAgroup

suggesting successful establishment of a rat model of RA. The results of immunohistochemistry

q RT-PCR

and Western blot all indicated that the expression level of CCR5 in synovial tissue was substantially higher in theRA group than in the control group

which was consistent with the results of bioinformatics analysis. Conclusion:CCR5 expression is high in RA patients and RA rats. It is feasible to use bioinformatic and experimental approachesto verify the genetic and histological evidence for the involvement of CCR5 in the development and progression ofRA. This study provides a theoretical basis for the follow-up study of the mechanism of action of CCR5 using a ratmodel of RA.