The chemoattraction of lymphocytes by rheumatoid arthritis–synovial fluid is not dependent on the chemokine receptor CCR5

B Santiago, M Galindo, M Rivero, M Brehmer… - Rheumatology …, 2002 - Springer
B Santiago, M Galindo, M Rivero, M Brehmer, I Mateo, J Pablos
Rheumatology international, 2002Springer
Objective. The objective was to study the potential role of the chemokine receptor CCR5 in
the chemoattraction of lymphocytes by rheumatoid arthritis synovial fluid (RA-SF). Methods.
The expression of the CCR5 receptor was studied by flow cytometry. Chemotaxis of
peripheral blood lymphocytes in response to RA-SF was analyzed on transmigration
chambers. Chemotaxis of immortalized lymphocytes from individuals homozygous for the
Δ32 deletion of the CCR5 gene (CCR5–/–) was analyzed. The effect of a neutralizing anti …
Objective
The objective was to study the potential role of the chemokine receptor CCR5 in the chemoattraction of lymphocytes by rheumatoid arthritis synovial fluid (RA-SF).
Methods. The expression of the CCR5 receptor was studied by flow cytometry. Chemotaxis of peripheral blood lymphocytes in response to RA-SF was analyzed on transmigration chambers. Chemotaxis of immortalized lymphocytes from individuals homozygous for the Δ32 deletion of the CCR5 gene (CCR5–/–) was analyzed. The effect of a neutralizing anti-CCR5 antibody on the migration of CCR5+/+ cells was also studied.
Results. We confirmed an increase in the proportion of CCR5-expressing lymphocytes in RA-SF and a preferential migration of CCR5+ lymphocytes toward RA-SF in vitro. CCR5–/– lymphocytes showed decreased chemotactic responses to the chemokine MIP-1β but not to RA-SF. The chemotactic responses of CCR5+/+ lymphocytes to RA-SF were not modified by anti-CCR5 neutralizing antibody.
Conclusions. We confirm a preferential accumulation of CCR5-expressing lymphocytes into RA-SF. However, the chemotactic responses of lymphocytes to RA-SF were not dependent on a functional CCR5 receptor, suggesting that CCR5 is a marker of a lymphocyte subset rather than a specific mediator of chemotactic responses to chemokines in RA-SF.
Springer