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Related Experiment Video

Updated: May 8, 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

ABIN1 dysfunction as a genetic basis for lupus nephritis.

Dawn J Caster¹, Erik A Korte, Sambit K Nanda

¹Departments of Medicine.

Journal of the American Society of Nephrology : JASN

|August 24, 2013

Summary

Genetic variants in the TNIP1 gene are linked to lupus nephritis risk. This suggests TNIP1 dysfunction may contribute to lupus nephritis development by altering immune cell signaling pathways.

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Area of Science:

Immunology
Genetics
Nephrology

Background:

The genetic basis of lupus nephritis, a severe complication of systemic lupus erythematosus, remains unclear.
Nuclear factor-kappa B (NF-κB) signaling is implicated in lupus pathogenesis.
Previous studies showed ABIN1 dysfunction enhances NF-κB and mitogen-activated protein kinase (MAPK) activation in immune cells.

Purpose of the Study:

To investigate the role of ABIN1 dysfunction in lupus nephritis development.
To examine the association of TNIP1 gene single-nucleotide polymorphisms (SNPs) with lupus nephritis in diverse populations.

Main Methods:

Genotyping of five TNIP1 SNPs in European-American, African American, Asian, Gullah, and Hispanic participants from the Large Lupus Association Study 2.
Comparison of SNP frequencies between systemic lupus erythematosus patients with and without nephritis, and with healthy controls.

Main Results:

ABIN1[D485N] mice developed progressive glomerulonephritis (GN) resembling human lupus nephritis.
Significant associations between TNIP1 SNPs and lupus nephritis were found: rs7708392 in European Americans and rs4958881 in African Americans.
rs7708392 showed a stronger association with lupus nephritis in European Americans when compared to healthy controls.

Conclusions:

Variants in the TNIP1 gene are associated with an increased risk of lupus nephritis.
ABIN1 dysfunction may contribute to lupus nephritis pathogenesis through dysregulated NF-κB and MAPK signaling.