Systemic Lupus Erythematosus (SLE) – Preclinical Models of Autoimmune Systemic Disease

Systemic Lupus Erythematosus (SLE) is a complex, chronic autoimmune disease characterized by multisystem inflammation, production of autoantibodies (especially anti-dsDNA), and immune complex deposition that can lead to glomerulonephritis, arthritis, skin lesions, and hematologic abnormalities. SLE pathogenesis involves dysregulation of both innate and adaptive immunity, with key roles for B cells, T cells, type I interferons, and complement activation.

At Redoxis, we offer a selection of in vivo models that reflect different aspects of SLE pathophysiology—ranging from spontaneous disease in genetically predisposed strains to inducible models for mechanistic and interventional studies. These models support efficacy evaluation of therapies targeting B cell activity, autoantibody production, T cell help, cytokine signaling, and immune complex-mediated tissue damage.

The pristane-induced lupus model is established in C57BL/6 or BALB/c mice by a single intraperitoneal injection of the hydrocarbon pristane. Over time, animals develop lupus-like features, including production of anti-dsDNA and other autoantibodies, proteinuria, glomerulonephritis, and systemic inflammation.

Disease is driven by innate immune activation, type I interferon production, and B cell autoimmunity. This model closely mimics many features of human SLE and is particularly useful for studying interferon signaling, autoantibody generation, and renal involvement.

Key Features:

  • Induced by intraperitoneal pristane injection
  • Development of autoantibodies (anti-dsDNA, anti-Sm)
  • Proteinuria and lupus nephritis
  • Involvement of type I IFN and TLR signaling pathways
  • Suitable for long-term efficacy studies and immune profiling
  • Compatible with flow cytometry and ex vivo restimulation assays from spleen and lymph nodes

The NZB/W F1 hybrid mouse spontaneously develops lupus-like disease with age, including high levels of anti-dsDNA antibodies, severe glomerulonephritis, and reduced survival. This genetically driven model is ideal for testing therapies that modulate B cell responses, immune complex deposition, and chronic kidney inflammation.

Key Features:

  • Spontaneous and progressive lupus-like disease
  • High-titer anti-dsDNA autoantibodies
  • Glomerulonephritis and proteinuria
  • Useful for evaluating long-term disease-modifying therapies
  • Translationally relevant for late-stage SLE pathology

The MRL/lpr mouse spontaneously develops severe systemic autoimmune disease driven by defective lymphocyte apoptosis, resulting in chronic immune activation, autoantibody production, lymphoproliferation, and multi-organ inflammation. The model displays several key features of human systemic lupus erythematosus (SLE), including glomerulonephritis, skin inflammation, and expansion of activated immune cell populations, making it highly valuable for evaluating therapies targeting systemic autoimmunity and lupus-associated tissue pathology.

Key Features:

  • Spontaneous and progressive lupus-like disease
  • Defective Fas-mediated apoptosis leading to systemic immune dysregulation
  • High levels of autoantibodies, including anti-dsDNA antibodies
  • Severe glomerulonephritis, proteinuria, and lymphoproliferation
  • Suitable for evaluating therapies targeting T- and B-cell responses, cytokine signaling, and chronic inflammation
  • Translationally relevant for systemic autoimmune disease and lupus nephritis

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Inquiries? Questions?

Nina Woodworth

COO