Chemokines regulate a wide array of physiological and pathological processes, including physiological trafficking, inflammation, hematopoiesis, angiogenesis, tumor growth, and human immunodeficiency virus (HIV) infection (1,2). All of these functions are mediated by signaling through seven-transmembrane domain G-protein-coupled receptors expressed on the target cell membrane. The coordinated expression of chemokines and their receptors define patterns of leukocyte trafficking during physiological immune surveillance and inflammation. Discrete tissue-committed subpopulations of circulating naive and memory T-cells can be distinguished, in part, by their expression of chemokine receptors. Whereas physiological trafficking is characterized by the homing of such receptor expressing cells to those tissues where cognate ligands are constitutively produced, the situation during local inflammation is intricate. A series of in vitro studies has demonstrated that Th1 and Th2 cells express distinct sets of chemokine receptors that might regulate the recruitment and localization of these cells to inflammatory sites (3,4). CXCR3 and CCR5 have been associated with the Th1 cytokine profile (5,6), whereas CCR3, CCR4, and CCR8 have been associated with the Th2 phenotype (7–10). Selective recruitment of subsets of CD4⁺ effector T-cells into sites of inflammation may contribute to the development of different pathological conditions (11,12). It is still a matter of speculation whether the infiltration of tissues by T-cells is contingent on the function of inflammatory chemokine receptors or whether the expression of such receptors is upregulated during tissue infiltration, therefore supporting the retention of T-cells in the tissue.