Short and long term outcome of renal transplantation are determined by acute and chronic rejection processes. In acute transplant rejection, expression of chemokines occurs in different renal compartments where it is triggered through various stimuli e.g. brain death, ischemia, reperfusion, and HLA-mismatch. The induction of chemokine expression precedes the process of organ recovery and extends well into the late course of clinical allograft injury. Chemokines function mainly as chemoattractants for leukocytes, monocytes, neutrophils, and other effector cells from the blood to sites of infection or damage. Chemokines are also important in angiogenesis and fibrosis and can have anti-inflammatory functions. The study of chemokine biology in transplantation has broadened the understanding of acute and chronic transplant dysfunction. Data suggest that relatively few chemokine receptors play central roles in these developments, and chemokine blockade, either non-selective or specific, has shown promising results in experimental transplantation and is currently being investigated in human trials.