In the search for new treatments for human inflammatory disease, antagonism of chemokine receptors by small molecules is an attractive goal. Although there are overlapping patterns of expression of chemokine receptors between leucocyte types, an investigation of the chemokine responsiveness of cells important in allergic inflammation, such as the eosinophil and the basophil, is beginning to uncover how selective recruitment may be regulated. The story of the eotaxin receptor, CCR3, and its central role in allergic inflammation illustrates that therapeutic antagonism of these pathways is imminently achievable.

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