T-cells accumulate within the rheumatoid arthritis synovium. The mechanism is unclear. This study investigated the possible role chemokines and their receptors may play in the accumulation in this T-cell accumulation. CXCR4 receptors are preferentially found on naive CD45RA+/RO- T-cells, and once differentiated, CXCR4 expression is downregulated. Because T-cells within the rheumatoid synovium are highly differentiated (CD45RO+/Rb^dull), they would be expected to have low CXCR4 expression. However, these investigators found increased expression of CXCR4 receptor on differentiated T-cells in rheumatoid synovium. This study sought to identify possible factors found within the rheumatoid joint that may be involved in the induction of CXCR4 on T-cells.

Results: After screening a large panel of cytokines on primed CD4+ T-cells, IL-2, IL-10 and IL-15 were found to induce a two-fold increase in CXCR4 expression, while TGF-binduced a 10-fold increase. Concentrations of cytokines used were similar to that found in inflamed synovial tissue. That the induced CXCR4 was functional was confirmed by its ability of SDF-1a(the chemokine that binds CXCR4) to induce adhesion of synovial fluid T cells to ICAM-1 and fibronectin.

Editorial Comment: These data suggest that inappropriate retention of T-cells at sites of chronic inflammation within the synovium may be due to the persistent induction of CXCR4 receptor expression on T-cells by TGF-b. The relevance of these in vitro studies to the in vivo environment of the joint remains to be investigated.

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