Key Words

and require renal replacement therapy, the latter being associated with signifi cant mortality, a lower quality of life, and high costs for national health systems. Thus, new treatment strategies that slow down, halt or even revert progressive renal damage are requested. Current treat-ments for chronic renal failure target to correct renal he-modynamics, proteinuria, high blood pressure, hyper-parathyroidism or to avoid nephrotoxic drugs and nico-tine abuse. A general role of immunosuppressive drugs in chronic kidney disease is not established, because of lack of effi cacy or unacceptable side effects of systemic immu-nosuppression. Many types of chronic kidney diseases are character-ized by an accumulation of interstitial leukocytes. Infi l-trating leukocytes are a major source for proinfl amma-tory and profi brotic cytokines and are therefore critical for mediating fi broblast proliferation, differentiation into myofi broblasts, matrix production, and tubular atrophy [1]. Thus, interfering with renal leukocyte recruitment may represent a valuable strategy to reduce renal infl am-mation, tissue remodeling, and progressive loss of renal function. During the past decade we and others have un-raveled the role of chemokines and chemokine receptors that direct circulating leukocytes into the damaged kid-ney, which was recently reviewed in detail [2]. In this ar-ticle, we focus on chemokine receptor CCR1 that was identifi ed from a group of other chemokines to play a critical role for interstitial leukocyte recruitment