What determines the type of cellular infiltrate in tissue injury? During the last 100 years pathologists have noted that etiolog-ically different and specific types of inflammatory reactions are associated with infiltration by specific subsets of inflammatory cells. Recent experimental and clinical observations in various forms of kidney diseases have highlighted the importance of interactions of specific leukocyte populations such as neutrophils, monocytes/macrophages and T cells with local renal cells in the disease process (for this review leukocytes are defined as any type of white blood cell)[1]. These studies also demonstrate how the recruitment of specific inflammatory cells to sites of renal injury contributes to both the acute and chronic phase of the specific disease. Conditions that determine the type of cellular infiltrate at the site of injury include:(1.) the local production and release of chemotactic factors; and (2.) activation of inflammatory cells, endothelium and surrounding cells resulting in the expression of adhesion molecules such as selectins and integrins on both the infiltrating inflammatory cells and the local cells. Previously, several general chemotactic factors have been iden-tified. These included the complement split product C5a, the formyl methionyl peptides (fMLP), leukotriene B4 and platelet activating factor (PAF). While these factors play a substantial role in inflammatory reactions they lack a leukocyte cell-type specificity. The enigma of leukocyte subtype specificity was resolved by the discovery of the superfamily of chemotactic cytokines, named chemokines, where each chemokine exhibits a rather restricted and selective pattern of leukocyte attraction [2, 31. Itis important to stress that chemokines are generated and released locally and are destined for local action. Chemokines appear not to be designed to function systemically, as their systemic administration or general overexpression in transgenic mice will not always lead to the expected phenotypic effects [4]. Thus far, numerous experimental studies and tissue evaluation of patients with a variety of inflammatory diseases of various organs including the kidney support an important role for chemokines in the specific type of leukocyte infiltration [3, 5]. The recent suggestion that chemokines may contribute to slow progression of the HIV infection and the very recent identification of chemokine receptors as docking molecules for HIV infection obviously add tremendous excitement and significance to chemo-kine research [6—8].