title: Animal models of rheumatoid arthritis and related inflammation.
abstract: The major, extensively studied, experimentally-induced rat and mouse models of arthritis with features resembling rheumatoid arthritis are reviewed here. Etiopathogenetic studies that were recently published are emphasized. In summary, multiple triggering stimuli can induce disease in genetically-prone strains of inbred rats and mice. Multiple genetic loci, including both MHC and non-MHC, regulate disease expression in these animals. By comparison with other models of autoimmune disease, clustering of regulatory loci within and among species is increasingly becoming evident. At the cellular level, both innate and acquired immune systems are involved in the disease manifestations. At the molecular level, unbalanced chronic production of tumor necrosis factor-alpha (TNF-alpha), interleukin (IL)-1, IL-6 and IL-12, as opposed to IL-4 and IL-10, is correlated with arthritis disease susceptibility and severity.
authors: Inflammatory Joint Diseases Section, Arthritis and Rheumatism Branch, National Institute of Arthritis and Musculoskeletal and Skin Diseases, National Institute of Health, Building 10, Room 9N240, 9000 Rockville Pike, Bethesda, MD 20892, USA.
authors: B
authors: B
authors: Joe
authors: M M
authors: MM
authors: Griffiths
authors: E F
authors: EF
authors: Remmers
authors: R L
authors: RL
authors: Wilder
mesh_terms: D000818:Animals; D016918:Arthritis, Reactive / Q000209:etiology* / Q000503:physiopathology*; D001172:Arthritis, Rheumatoid / Q000209:etiology* / Q000503:physiopathology*; D002358:Cartilage, Articular / Q000378:metabolism; D004195:Disease Models, Animal; D005260:Female; D006801:Humans; D008297:Male; D051379:Mice; D008811:Mice, Inbred DBA; D008822:Mice, Transgenic; D051381:Rats; D012680:Sensitivity and Specificity; D012720:Severity of Illness Index; D013045:Species Specificity