Animal models for nervous system disease in systemic lupus erythematosus.
Animal models have much to teach us about nervous system dysfunction in SLE. It should be stressed that the murine strains described in this review have variable expression in the onset and severity of clinical and serological features, perhaps making them more like a heterogeneous human population with SLE. With this in mind, studies involving animal models like those involving human subjects should use a sample size that ensures adequate power. It is not surprising that studies that use sample sizes as low as four to five animals per group would find discrepant results, especially in outcomes that are measured prior to the terminal phases of the disease. Similar to human SLE patients, murine models have systemic autoimmune as well as neurological manifestations. Studies with murine models must continue to consider some type of SLE disease activity measures in order to control for the effects of systemic disease on nervous system dysfunction. Because of the short time window between the earliest evidence of neurologic dysfunction and severe autoimmune disease manifestations, especially in MRL/lpr mice, the disease acceleration model may allow a more careful dissection of how immunological events are related to nervous system dysfunction. Alternatively, the study of MRL/lpr mice ultraearly (e.g., 3 weeks of age) could also provide invaluable information about the first events leading to nervous system dysfunction in SLE. Both approaches promise to identify predictors of specific nervous system manifestations that may suggest novel and more specific therapeutic interventions.
Brey
R L
RL
Department of Medicine, University of Texas Health Science Center at San Antonio 78284-7883, USA. brey@uthscsa.edu
Sakic
B
B
Szechtman
H
H
Denburg
J A
JA
D000818:Animals; D004195:Disease Models, Animal; D008180:Lupus Erythematosus, Systemic / Q000150:complications / Q000662:veterinary*; D051379:Mice; D008817:Mice, Mutant Strains; D009422:Nervous System Diseases / Q000209:etiology / Q000662:veterinary*; D012376:Rodent Diseases / Q000628:therapy*