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:
• IFNg 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 up-regulated (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.

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