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Updated: Jun 2, 2026
Analyses of Proteinuria, Renal Infiltration of Leukocytes, and Renal Deposition of Proteins in Lupus-prone MRL/lpr Mice
Published on: June 8, 2022
Chromatin as a target antigen in human and murine lupus nephritis
Annica Hedberg1, Elin Synnøve Mortensen, Ole Petter Rekvig
1Molecular Pathology Research Group, Institute of Medical Biology, Faculty of Health Science, University of Tromsø, N-9037 Tromsø, Norway.
Abstract:
The present review focuses on pathogenic molecular and transcriptional events in patients with lupus nephritis. These factors are renal DNaseI, exposed chromatin fragments and the corresponding chromatin-reactive autoantibodies. Lupus nephritis is the most serious complication in human systemic lupus erythematosus, and is characterised by deposition of chromatin fragment-IgG complexes in the mesangial matrix and glomerular basement membranes. The latter deposition defines end-stage disease. This event is stringently linked to a renal-restricted shutdown of expression of the DNaseI gene, as determined by loss of DNaseI mRNA level and DNaseI enzyme activity. The major aim of the present review is to generate new therapeutic strategies based on new insight into the disease pathogenesis.
Insights
Lupus nephritis involves kidney damage from chromatin fragments and autoantibodies. A key factor is the shutdown of the DNaseI gene in the kidneys, offering new therapeutic targets.
Area of Science:
- Nephrology
- Immunology
- Molecular Biology
Background:
- Lupus nephritis is a severe complication of systemic lupus erythematosus.
- It involves the deposition of chromatin fragment-IgG complexes in the kidneys.
- This deposition is linked to end-stage renal disease.
Purpose of the Study:
- To review pathogenic molecular and transcriptional events in lupus nephritis.
- To explore the role of renal DNaseI, chromatin fragments, and autoantibodies.
- To identify new therapeutic strategies based on disease pathogenesis.
Main Methods:
- Review of existing literature on lupus nephritis pathogenesis.
- Analysis of molecular mechanisms involving DNaseI gene expression.
- Investigation of chromatin fragment and autoantibody interactions.
Main Results:
- Renal DNaseI, exposed chromatin fragments, and autoantibodies are key pathogenic factors.
- Kidney-specific DNaseI gene expression shutdown is linked to disease progression.
- Chromatin deposition in the mesangial matrix and glomerular basement membranes defines end-stage disease.
Conclusions:
- Understanding these molecular events is crucial for lupus nephritis treatment.
- Targeting DNaseI gene expression or related pathways may offer therapeutic benefits.
- New strategies can be developed based on insights into lupus nephritis pathogenesis.
