Lupus nephritis (LN) occurs in more than one-third of patients with systemic lupus erythematosus. Its pathogenesis is attributed to the glomerular deposition of immune complexes as well as to imbalance of the cytokine homeostasis. In this context, high production of cytokines and chemokines by dendritic cells (DCs) may concur to LN. In addition, urinary cytokine excretion may reflect the accumulation of DCs within glomeruli. DCs are differentiated in both myeloid and plasmacytoid (p) subsets in relation to their typical antigen and chemokine expression. Both subsets migrate in response to chemotactic stimuli because pDCs are susceptible to IL-18 expressed by resident glomerular cells. pDCs bear the IL-18R, and it is conceivable that DCs migrate to the kidney under the attraction of IL-18. Therefore, the depletion of DCs reflects the inflammation severity in LN, whereas measurement of Th1 cytokines may represent an effective tool for monitoring the onset of LN.