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Systemic Lupus Erythematosus (SLE) Models

Utilize robust, spontaneous SLE models which more closely represent human disease.

Key Benefits

  • Advance SLE agent development with robust in vivo models
  • Determine efficacy and response to treatment.
  • Select qualified lupus lead agents.

Select preclinical models with diverse mechanisms capturing many key characteristic clinical and pathologic features of SLE including:

  • MRL/Faslpr spontaneous model
  • NZB/W spontaneous model.

MRL/Faslpr spontaneous model of SLE

  • Spontaneous onset starting at 9-10 weeks of age, developing over 7-9 weeks.
  • Major phenotype/characteristics:
    • dramatic lymphoproliferation and lymphadenopathy
    • splenomegaly
    • glomerulonephritis (subacute, proliferative) and proteinuria
    • skin lesions
    • expansion of CD3+CD4-CD8- T cells
    • no interferon signature.

NZB/W spontaneous model of SLE

  • Spontaneous onset starting around 22-23 weeks of age, developing over 12-13 weeks.
  • Major phenotype/characteristics:
    • splenomegaly
    • glomerulonephritis (subacute, proliferative) and proteinuria
    • persistence of long-lived autoreactive plasma cells
    • interferon signature.

Major endpoints for assessment:

  • Body weight.
  • Skin lesions (in MRL/Faslpr).
  • Proteinuria.
  • Spleen, kidney, and lymph node size/weight.
  • Cytokine levels.
  • Blood serum anti-dsDNA antibody levels.
  • Blood urea nitrogen (BUN) levels.
  • FACS analysis of immune cell populations.
  • Kidney histopathology and IHC staining for C3 and IgG levels.



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