Eosinophils are cellular hallmarks of allergic inflammation, and investigations to delineate the mechanisms responsible for eosinophil recruitment and activation have been important for understanding the pathogenesis of allergic diseases. Since the early finding that anaphylactically-challenged guinea pig lungs released an eosinophil chemoattractant activity (then termed, eosinophil chemotactic factor of anaphylaxis)(1), the search has been on to identify the primary chemoattractant agent with specificity for eosinophils. Over the years many agents have been identified that exhibit eosinophil chemoattractant activity (2), but more recently interest has focused on the chemokine, eotaxin. Eotaxin was first identified as the dominant eosinophil-chemoattractant in a guinea pig model of allergic airway inflammation (3), promoting both local eosinophil recruitment to the lung and, in cooperation with interleukin (IL)-5, rapid mobilization of a pool of bone marrowretained, matured eosinophils (4). Subsequently, human eotaxin has been cloned, and its synthesis (mRNA and protein) demonstrated in allergic diseases, including asthma (5–7).

Chemokines are members of a very large superfamily of homologous small (8 to 10 kDa) peptides that typically regulate the chemoattraction of leukocytes. Chemokines are subdivided into families based on the relative positions of their first two cysteine residues. The CC (or) chemokines have their cysteines located adjacent to each other and, in general, are chemoattractants not for neutrophils but for eosinophils, basophils, monocytes, and lymphocytes. Human eotaxin, an 8.4 kDa CC chemokine, is not the only CC chemokine with preferential activities on eosinophils. More recently, two additional new human eosinophil selective CC chemokines have been described and named eotaxin-2 (8) and eotaxin-3 (9, 10). Strikingly, in contrast to their similar functional chemoattractant activities, the overall sequence identities of these three members of eotaxin subfamily are only 34–38%. On the other hand,