Animal models of autoimmune conditions are, in similarity with the humane disease they mimic, complex diseases dependent on both genetic and environmental factors. Different models mimic different aspects of the human disease, requiring the need for multiple models for each indication and thorough knowledge about the models and MoA, for study planning and interpretation.
Models of Rheumatoid Arthritis (RA)
Development of novel drugs for treatment of chronic inflammatory diseases is to a large extent dependent on the availability of good experimental in vivo models for preclinical tests and identification of new targets.
Although a single RA in vivo model cannot mirror the complexity of disease there are a number of good animal models for RA, each defining different aspects of the human disease.
Models of Multiple Sclerosis (MS)
Experimental Autoimmune Encephalomyelitis (EAE) is the most commonly used model for MS, a human inflammatory demyelinating disease of the central nervous system (CNS), and resembles disease in many aspects. EAE is an antigen driven autoimmune model in which immunization against myelin antigens elicits strong T cell responses, which initiates its pathology with CNS myelin destruction. EAE is induced by immunization with CNS tissue or myelin peptides. Different immunization protocols result in varying disease characteristics.
Models of Guillain-Barré Syndrome (GBS)
Guillain-Barré syndrome (GBS) and chronic inflammatory demyelinating polyradiculoneuropathy (CIPD) are autoimmune-mediated inflammatory diseases of the peripheral nervous system (PNS). The umbrella term of GBS is several variants with distinct clinical and pathological features. The most frequent from of GBS in the western countries is the acute inflammatory demyelinating polyneurophaty (AIPD), characterized by acute ascending paralysis, hyporeflexia with variable sensory involvement and histopathologically by mononuclear infiltrates and segmental demyelination. Chronic inflammatory demyelinating polyneuropathy (CIPD) can be relapsing-remitting or progressive. Experimental Autoimmune Neuritis (EAN) is a widely accepted model of GBS and is induced by immunization with peripheral myelin antigens.
Models of Systemic Lupus Erythematosus (SLE)
Systemic Lupus Erythematosus is a highly complex and heterogenous autoimmune disease more often affecting women in their child-bearing years. The disease is characterized by circulating autoantibodies to nuclear antigens (ANAs) such as anti-Sm and anti-dsDNA, immune complex formation and inflammation in multiple organs. The inflammatory response can lead to tissue damage. Animal models for SLE composes of both induced, spontaneous and genetically modified models. These models, to varying degrees, mimic the hallmarks of the human disease and are good tools for evaluation of efficacy of novel therapies.
Models of acute sepsis (LPS induced)
Administration of LPS to mice induce an acute inflammatory response similar to the response occurring during early stages of septic shock with a massive release of cytokines and chemokine. This is a short and cost-effective model for evaluation of anti-inflammatory properites.
Models of Psoriasis and Psoriatic Arthritis
Psoriasis is one of the most common autoimmune diseases resulting in chronic skin inflammation and systemic manifestations dependent on both genetic and environmental factors. Ps is characterised by a thickening of the epidermis and immune infiltrates throughout the dermis and epidermis, causing skin lesion that affect quality of life. Many patients affected by psoriasis also develop inflammation in other organs, often joints as in psoriatic arthritis (PsA). To study the disease pathogenesis, animal models is a good tool.
Models of Parkinson´s disease
Redoxis provides different and complementary mouse models of PD, one of which is the unilateral intrastriatal lesion with the 6-Hydroxydopamine (6-OHDA) toxin to mimic disease hallmark. The use of toxin-mediated models like the 6-OHDA has been widely used in rodent models of Parkinson’s disease as it can reliably reproduce the selective dopaminergic loss.