However, very surprisingly, CXCR3 defect led neither to reduced kidney cellular infiltrates nor to diminished glomerulonephritis in those animals, although, as we show in the present study, all elements (receptor/ligand/pathology-involved cells) are gathered to support a pathogenic role of this inflammation-related axis in the lupus-associated renal disease. The gene discussed is CXCR3; the disease is glomerulonephritis.