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. |