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Updated: May 15, 2026
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Toll-like receptor 3 ligand, polyIC, induces proteinuria and glomerular CD80, and increases urinary CD80 in mice
Takuji Ishimoto1, Michiko Shimada, Garcia Gabriela
1Division of Renal diseases and Hypertension, University of Colorado Denver, Aurora, CO, USA. Takuji.Ishimoto@ucdenver.edu
Background:
We have reported that children with biopsy-proven minimal change disease (MCD) express CD80 (also known as B7.1) in their podocytes and excrete high levels of CD80 in their urine during active nephrotic syndrome. We also reported that polyIC, a Toll-like receptor 3 ligand, increases CD80 mRNA and protein expression in cultured human podocytes dose-dependently, with actin re-organization and a reduction in synaptopodin expression.
Methods:
To determine the effect of polyIC in the kidney, we subjected mice to systemic injection of polyIC or phosphate buffered saline.
Results:
Mice injected with polyIC developed significant proteinuria with increased urinary CD80 excretion. Glomeruli from mice injected with polyIC were normal by light microscopic examination, but showed increased CD80 production in podocytes by immunofluorescence staining. In isolated glomeruli from mice injected with polyIC, expressions of CD80 and interleukin 10 significantly increased with a mild non-significant increase in CTLA-4, and synaptopodin expression decreased significantly.
Conclusions:
Our study demonstrates that systemically administered polyIC can induce transient proteinuria and urinary CD80 excretion with an increase in CD80 production in podocytes, increased glomerular CD80 and reduced synaptopodin expression. These findings may be relevant to the pathogenesis of proteinuria in MCD.
Insights
Systemic administration of polyinosinic:polycytidylic acid (polyIC) induces transient proteinuria and increases CD80 (B7.1) in kidney podocytes. This finding may explain minimal change disease (MCD) pathogenesis.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Children with minimal change disease (MCD) exhibit podocyte CD80 (B7.1) expression and urinary CD80 excretion during active nephrotic syndrome.
- Polyinosinic:polycytidylic acid (polyIC), a Toll-like receptor 3 ligand, upregulates CD80 in cultured human podocytes, affecting actin and synaptopodin.
Purpose of the Study:
- To investigate the in vivo effects of systemic polyIC administration on kidney function and CD80 expression in mice.
Main Methods:
- Mice received systemic injections of polyIC or phosphate-buffered saline.
- Kidney function, urinary CD80 levels, and glomerular protein expression were analyzed.
Main Results:
- PolyIC injection led to significant proteinuria and increased urinary CD80 excretion.
- Immunofluorescence revealed increased podocyte CD80 production in polyIC-treated mice.
- Glomeruli showed elevated CD80 and interleukin-10, with decreased synaptopodin expression.
Conclusions:
- Systemic polyIC induces transient proteinuria, increased urinary CD80, and altered glomerular protein expression.
- These polyIC-induced changes in podocytes may contribute to the pathogenesis of proteinuria in minimal change disease.
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