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. |