Lupus nephritis is a common solid organ manifestation of systemic lupus erythematosus (SLE). The disease is tightly linked to the production of autoantibodies and circulating immune complexes, i.e. immune complex glomerulonephritis. In this process chemokines mediate multiple biological effects, e.g. orchestrating proinflammatory microenvironments, the recruitment of immune cell subsets into the kidney, as well as the local activation of such immune effector cells. Autoimmune mice with targeted deletions of certain single chemokines or chemokine receptors are protected from renal autoimmune tissue injury. Interventional studies with specific antagonists against certain chemokines and chemokine receptors further support these findings. In this review we summarise the available experimental and human data on the expression and functional role of chemokines and chemokine receptors in lupus nephritis.