In response to renal immune complex accumulation in systemic lupus erythematosus (SLE), monocytes, T lymphocytes, and neutrophils infiltrate the kidney and mediate tissue injury and renal dysfunction. Chemotactic factors induced by immune complexes are responsible for recruiting these inflammatory cells to the kidney. Considerable attention has focused on the role of the chemokine network in regulating renal leukocyte recruitment in autoimmune glomerular diseases. In animal models of SLE nephritis, intervention studies directed at chemokines or chemokine receptors have provided definitive proof that specific chemokines are involved in the pathogenesis of renal inflammation. These same chemokines and chemokine receptors are expressed in the kidney during human SLE nephritis, and correlate with markers of renal injury and inflammation. This review will describe and integrate the animal and human data to build a case for targeting the chemokine network as a novel approach to the treatment of SLE nephritis. Anti-chemokine therapies hold the promise of efficacy with fewer adverse side-effects than the non-specific immunosuppression regimens currently in use.