| Reference | Species | Treatment study | Renal compartment | Brief description
          of the main results | Correlation with
          clinical/histological parameters | 
      
        | Peterson et al,
          2004 (1) | Human | No. | Glomerular
          (laser-capture
          microdissection) | • Four main gene clusters of up-regulated
          genes: 1. Type I IFN-response element
          genes; 2. Myelomonocytic lineage and
          inflammatory cell genes; 3. B-cell genes; 4.
          ECM and glomerulosclerosis genes. • One main cluster of down-regulated
          genes included cellular growth,
          differentiation, endothelial cell proliferation
          and angiogenesis genes.
 | There was a tendency for the genes
          from the IFN-inducible gene cluster to be
          associated with less crescent formation,
          whereas transcripts from the B-cell
          infiltration cluster were associated with more
          crescents. | 
      
        | Liu et al, 2006 (2)
 | MRL/lpr
          mouse | No. | Whole kidneys | Findings in this model recapitulated some
          in humans: • IFNγ pathway members are dysregulated
          and important in the development of LN in
          this model.
 • mRNA expression of genes implicated in
          inflammatory pathways are also altered in
          LN (e.g. cytokines, antigen presentation,
          …)
 | Not done. | 
      
        | Teramoto et al,
          2008 (3) | MRL/lpr
          mouse | Yes. (Prednisone)
 | Glomerular
          (laser-capture
          microdissection) | Findings in this model recapitulated some
          in humans: • Genes related to Th1 cells are upregulated
          (chemokines, chemokine
          receptors, complement, coagulation, etc.).
          IL-27 was highlighted.
 • Effect of glucocorticoid treatment
          (Prednisone): decrease of infiltrating
          cell number, glomerular injury and
          inflammatory gene expression.
 | Not done. | 
      
        | Reddy et al,
          2008 (4) | NZB/W
          mouse | Yes. (Sirolimus)
 | Whole kidneys | • 387 genes were regulated during LN,
          associated with pathways such as antigen
          presentation, complement, IL-1 and IL10
          signaling pathways, Jak-Stat and MAP
          kinase pathways. • Many of them were decreased after
          treatment with the mTOR inhibitor
          sirolimus.
 | Not done. | 
      
        | Bethunaickan
          et al,
          2011 (5) | NZB/W | Yes.
          (Cyclophosphamide +
          CTLA4 Ig + anti-CD154
          Ab) | Renal F4/80hi cells | Activated renal macrophages contribute to
          renal damage in LN: • Transcripts from proinflammatory,
          regulatory, tissue repair/degradation
          pathways were overexpressed.
 • Those transcripts were reduced to their
          basal expression level after induction of
          remission by immunosuppressive therapy.
 | Not done. |