Study of human autoimmune disease presents the considerable problem of deciding whether the changes observed are the cause or consequence of the disease process. The use of animal models avoids this difficulty and their manipulative potential has yielded many valuable insights into the autoimmune process. The disease range of induced models now available covers a wide spectrum of human autoimmune diseases and, although differing in detail from the human conditions, they have been instrumental in clarifying basic pathogenic mechanisms and, perhaps more importantly, in demonstrating that multiple and converging pathways to autoimmune disease development exist. They have also demonstrated that, in addition to a specific triggering event, disturbances of normal regulatory function may be prerequisite for chronic, sustained autoimmunity.
Finally, despite the multifactorial nature of autoimmune disease clearly revealed by modeling, this approach also offers the prospect that autoimmune disease might be controlled by interfering with the final common pathways without necessarily eliminating all the anteceding immune abnormalities.
See also: Adjuvant arthritis; Anemia, autoimmune hemolytic in animal models; Autoantigens; Autoimmune disease, spontaneous experimental models; Autoimmunity; Contrasuppression; Experimental autoimmune encephalomyelitis (EAE); Idiotype network; Immunosuppression; insulin-dependent diabetes mellitus, animal models; Multiple sclerosis; Neuromuscular junction autoimmunity; Rheumatoid arthritis, animal models; T cell vaccination; Thyroid autoimmunity, experimental models; Transgenic animals.
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