Figure 7.

Overview of major mechanisms and effector pathways implicated in lupus nephritis pathogenesis emerging as targets of future therapies. Molecular network analysis followed by druggability assessment suggested key dysregulated gene modules involving “interferon”, “B cells”, “plasma cells”, “antigen presentation”, “protein synthesis”, and “extracellular matrix”. Aberrant transcriptomic signatures could be reversed by specific drugs, as schematically depicted. ALCAM, activated leukocyte cell adhesion molecule; Anti-PD-L1, antiprogrammed death-ligand 1; BTK, Bruton’s tyrosine kinase; CCR1, CC-motif chemokine receptor 1; cIAP1/2, cellular inhibitors of apoptosis 1/2; JAK2, Janus kinase 2; PI3K, phosphoinositide 3-kinase; TYK2, tyrosine kinase 2.