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Abstract
In this study we were interested in investigating the extent to which stimulation through a chemokine receptor could modulate TCR function. We report that splenic T cells exposed to secondary lymphoid‐tissue chemokine (SLC, CCL21) for 72, but not 2 or 24 hours, exhibited a decreased ability to produce IFN‐γ following CD3 crosslinking. Similar findings were observed with CCL2 and CCL5. The decrease in IFN‐γ production was not attributed to a decrease in T cell viability, was not accompanied with an increase in IL‐4 production, and could be induced using a G protein coupled receptor agonist indicating involvement of chemokine receptors. One explanation for these findings was that following chemokine exposure the T cells were less efficient at TCR capping and exhibited a decrease in ZAP‐70 protein expression. Consequently, these data indicate that CCL21 could modulate the function and expression of proteins necessary for T cell activation.