SLE is an autoimmune disease characterized by autoantibody production leading to immune complex (IC) formation and resulting in a variety of organ manifestations with a high prevalence of nephritis*.
SLE in humans is characterized by:
- Inflammatory lesions in skin, joints, kidneys, CNS and other
- The clinical manifestations are accompanied by autoantibodies diverse self-antigens, mainly but not exclusively derived from the cell nucleus.
It is a multisystem, antibody-mediated disorder apparently related to genetic and hormonal factors with antibody production responsive to environmental triggers that perhaps contribute to degradation of tolerance controls.
Pristane-induced lupus is a well-established model of murine lupus with demonstrated usefulness for evaluation of new therapies.
SLE Mouse Model
Animals: Balb/c mice, 8 week old, female
Single injection of 0.5 ml pristane
Readouts: BAL volume and cell counts, cytokines (e.g. IL-6, IL-10, IL-12 and IFN-1), anti-DNA Antibody (ELISA and Immunofluoresence), lung histology, immune complex deposition, arthritic effects, nephritic effects (urinary protein).
Anti-DNA antibodies are sensitive in SLE.
Immunofluoresence stained slides provide a visual record of treatment efficacy.
Pristane Model Results Antinuclear Antibodies
Immunofluoresence Staining on HEp-2 Cells
Mouse models of SLE are used to shed light on disease mechanisms and to test potential therapies. In drug development for treatment of SLE testing in mouse models is considered indispensable. Targets for prophylactic or therapeutic treatments have included cytokines, B-cells, T-cells and hormones reflecting the complex multi-organ involvement of this disease.
Current treatments for SLE usually involve the use of cytotoxic or immunosuppressive agents that can lead to infection** or cancer.
* Washington Biotechnology offers two animal models of nephritis for efficacy assessments of test materials.
**Enhanced susceptibility to infections caused by actions of a test compound may be evaluated using one of our mouse models for bacterial infection (Listeria or Candida).
REFERENCE: SLE from Mouse Models to Human Disease and Treatment, NIH Conference, September 2-3, 2010, Bethesda, Maryland, USA.
