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Updated: Dec 10, 2025

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

Complement Properdin Determines Disease Activity in MRL/lpr Mice.

Hasanain Alaridhee¹, Azzah Alharbi^1,2, Zeayd Saeed^1,3

¹Department of Respiratory Sciences, University of Leicester, Leicester LE1 9HN, UK.

Medicina (Kaunas, Lithuania)

|September 2, 2020

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Properdin deficiency significantly reduces lupus severity and kidney damage in mouse models. This suggests targeting properdin could be a novel therapeutic strategy for lupus nephritis.

Area of Science:

Immunology
Nephrology
Rheumatology

Background:

Systemic lupus erythematosus (SLE) involves immune complexes triggering complement activation, leading to glomerulonephritis.
Mouse models are crucial for preclinical evaluation of therapies targeting complement pathways in lupus.
Properdin, a positive regulator of complement, has an unstudied role in lupus nephritis severity.

Purpose of the Study:

To investigate the role of properdin in the pathogenesis and severity of lupus nephritis.
To assess the impact of properdin deficiency on disease manifestations in a lupus mouse model.

Main Methods:

Properdin-deficient mice were crossed with lupus-prone MRL/lpr mice.
Disease severity was evaluated by measuring anti-DNA antibody titers, inflammatory mediators (TNFα, BAFF), and renal function markers (serum creatinine).

Keywords:

lupus mouse model properdin

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Main Results:

Mice lacking properdin exhibited significantly lower anti-DNA antibody levels, TNFα, and BAFF compared to controls.
Properdin-deficient MRL/lpr mice showed reduced glomerulonephritis severity and lower serum creatinine levels.
These findings indicate a critical role for properdin in lupus nephritis progression.

Conclusions:

Properdin significantly contributes to the overall severity of lupus and the extent of glomerulonephritis in MRL/lpr mice.
Reduced autoantibody production, inflammation, and renal impairment in properdin-deficient mice highlight its pathogenic role.
Properdin inhibition presents a potential novel therapeutic target for managing lupus disease and its renal complications.