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.
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.
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.
Table 2: Renal transcriptional profiling of LN in chronological order, as assessed by microarray studies.