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Related Experiment Video

Updated: May 19, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Genetic approach to study lupus glomerulonephritis.

Yan Ge¹, Michael G Brown, Hongyang Wang

¹Department of Medicine and Center of Immunity, Inflammation and Regenerative Medicine, University of Virginia School of Medicine, Charlottesville, VA, USA.

Methods in Molecular Biology (Clifton, N.J.)

|August 31, 2012

Summary

Genetic factors influence lupus nephritis progression. Researchers identified specific quantitative trait loci (QTL) in a mouse model, significantly reducing disease severity and confirming separate genetic control for acute and chronic kidney inflammation.

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Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

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Published on: June 18, 2020

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Last Updated: May 19, 2026

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice

Published on: June 8, 2022

Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

Supervised Machine Learning for Semi-Quantification of Extracellular DNA in Glomerulonephritis

Published on: June 18, 2020

Area of Science:

Immunology
Genetics
Nephrology

Background:

Systemic lupus erythematosus (SLE) pathogenesis involves genetic and environmental factors.
Lupus nephritis, a severe SLE manifestation, causes kidney inflammation and function loss.
Understanding lupus nephritis progression is crucial for effective clinical treatment.

Purpose of the Study:

Identify genes controlling the development and progression of lupus nephritis.
Utilize a spontaneous mouse model (NZM2328) and a resistant strain (C57L/J) for genetic mapping.
Investigate the genetic basis of glomerulonephritis (GN) in SLE.

Main Methods:

Classical genetics and backcrossing of NZM2328 mice with C57L/J mice.
Quantitative trait loci (QTL) analysis to map genes controlling GN features (Agnz1, Agnz2, Cgnz1).
Development of a congenic strain (NZM23238.C57Lc1) to verify QTL linkage and genetic control.

Main Results:

QTLs associated with acute (Agnz1, Agnz2) and chronic (Cgnz1) GN were identified.
The congenic strain Lc1 showed markedly reduced development of both acute and chronic GN.
Further mapping supported separate genetic control for acute and chronic GN.

Conclusions:

Genetic factors significantly influence the development and progression of lupus nephritis.
Specific QTLs on mouse chromosome 1 play a role in controlling GN in this SLE model.
Acute and chronic phases of GN are regulated by distinct genetic mechanisms.