CXCL10 and lupus nephritis: Of note, a therapeutic option to modulate parenchymal renal cells (e.g., pTECs) with the aim of generating an antiinflammatory microenvironment in renal autoimmune diseases has recently been proposed (32), and multiple studies underscore the central role of the CXCL9/CXCL10-CXCR3 axis in the development of human and experimental immune-mediated kidney diseases, including ANCA-GN and lupus nephritis, by directing pathogenic effector T cells to the sites of inflammation, thus identifying this pathway as a promising therapeutic target (15, 18, 33–35).