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The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

The bm12 Inducible Model of Systemic Lupus Erythematosus SLE in C57BL/6 Mice

Published on: November 1, 2015

CD95 and the MRL-lpr Mouse Model.

Robin J Flynn¹

¹Department of Infection Biology, Institute of Infection & Global Health, University of Liverpool, 8 West Derby Street, Liverpool, L69 7BE, UK. Robin.Flynn@liverpool.ac.uk.

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

|January 13, 2017

Summary

This summary is machine-generated.

Mice lacking CD95 (Fas-ligand) develop lupus-like autoimmune disease. Researchers used heterozygote offspring to test a CD95L blocking peptide, offering a new model for studying autoimmune disease treatments.

Keywords:

CD95L Fas-L Faslpr Kidney damage Lupus MRL-lpr Mouse model of autoimmunity SLE T-cell

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Published on: January 7, 2019

Area of Science:

Immunology
Autoimmunity
Molecular Biology

Background:

CD95 (Fas-ligand) is crucial for regulating cell death.
Loss of CD95 function in MRL-lpr mice leads to spontaneous autoimmunity, including arthritis and glomerulonephrosis.
This strain serves as a valuable model for studying systemic lupus erythematosus (SLE).

Purpose of the Study:

To investigate the therapeutic potential of a CD95L blocking peptide.
To establish a novel experimental model using heterozygote MRL-lpr mice for studying lupus-like disease.
To evaluate the in vivo effects of CD95L blockade on autoimmune manifestations.

Main Methods:

Utilized heterozygote offspring of MRL-lpr mice.
Administered a CD95L blocking peptide in vivo.
Monitored the development and progression of lupus-like disease characteristics.

Main Results:

The study describes a method to utilize heterozygote offspring.
The CD95L blocking peptide was tested in this model.
This approach allows for in vivo study of CD95L's role in lupus-like disease.

Conclusions:

A novel model using heterozygote MRL-lpr mice was developed.
This model facilitates the study of CD95L blocking peptides in autoimmune disease.
The findings support further investigation into CD95L targeted therapies for SLE.