Much is still to be learned about immune & inflammatory pathways in LN1. A bioinformatic approach (LIMMA-DE & WGCNA) analyzed gene expression of LN biopsies microdissected for glomerulus and tubulointerstitum. Genes differing between LN & healthy individuals were interrogated for cell type specific gene signatures using GSVA validation of I- or T- Scope® analysis of immune or non-immune subsets. Podocytes are in WGCNA modules negatively correlated with WHO class. Genes were functionally characterized using BIG-C® and pathways elucidated using IPA®. LN has an immune cell signature in WGCNA modules positively correlated with WHO class (granulocytes, pDC, DC, myeloid cells, CD4+, & CD8+ Ts, Bs as well as pre- and post-switch PCs as indicated by IgM, IgD, and IgG1 HC genes). The presence of both Ig -κ & -λ as well as VL genes suggests polyclonal activation. Chemokines that mediate lymphocyte organization and/or recruitment into lupus kidney are present. Cytokine (TNF, CD40L, IL1β, IL2, IL6, IL12, IL17, IL23, & IL27) & signaling (PI3K,NF-κB,NF-AT, and p70S6K) pathways as well as proliferation and HDAC activity are evident. IPA® UPR analysis indicated ongoing signaling by cytokines such as TNF, IFNγ, IFNα, CD40L, IL1β, IL2, IL6, & IL17. Interestingly, connectivity analysis using LINCS/CLUE elucidated high priority drug targets such as IFNb (PF-06823859), IL12 (Ustekinumab) and S1PR(Fingolimod) that may prove to be good options for therapeutic intervention.