Abstract
The expression of chemokine receptors by dendritic cells (DCs) is a regulated phenomenon. The immature CD34 precursor-derived human DCs respond via CCR6 to MIP-3α, but following maturation, lose responsiveness to MIP-3α, and downregulate CCR6, while become responsive to MIP-3β. In the tonsil, MIP-3α is expressed in follicle-associated epithelium, whereas MIP-3β is expressed in T-cell areas. This suggests that DC maturation is associated with modulations of chemokine receptor expression that would direct immature DCs to peripheral areas, but on receipt of maturation signals they would be targeted to T cell areas. A variety of nonspecific stimuli can affect DC migration dramatically, possibly acting via a final common pathway involving TNF-α and IL-1. I.v. endotoxin induces a rapid increase in the numbers of DCs migrating in lymph from the intestine. An antigen needs to gain access to DCs to stimulate an immune response and the presence of DCs and their processes within intestinal epithelia may facilitate this interaction.
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