Rheumatoid arthritis experimental models

For some autoimmune diseases, little is known about environmental factors involved in the initiation or progression of the disease. For other diseases, however, considerable research has been conducted on one or more types of exposures. Most epidemiologic studies of environmental influences have focused on multiple sclerosis, rheumatoid arthritis, scleroderma, systemic lupus erythematosus, and small vessel vasculitis, but experimental studies using murine models of these diseases is limited (Table 25.1). 

Muller-Ladner U, Gay S. The SCID mouse—a novel experimental model for gene therapy in human rheumatoid arthritis. Drugs Today (Barcelona) 1999 35 379-88. 

To find out more about the possible role of cathepsin D in the pathological tissue damage of rheumatoid arthritis, we want to work with the chick embryo organ culture system, with an experimental arthritis model in rabbits, and with human tissue samples so we purified and studied the enzyme from each of the three species (1-3). 

Tissue-specific Galactosyltransferase Abnormalities in an Experimental Model of Rheumatoid Arthritis... 

We have investigated tissue-specific galactosyltransferase abnormalities in an experimental model of rheumatoid arthritis [41], The study focused on whether the observed pathophysiological similarities that develop in both the collagen induced experimental model of arthritis (CIA) and RA are associated with similar glyco-... 

Alavi A, Axford JS, Hay FC, Jones MG. Tissue-specific galactosyltransferase abnormalities in an experimental model of rheumatoid arthritis. Ann Med Intern (1998) 149(5) 251-260. Axford JS, Sumar N, Alavi A, Isenberg DA, Young A, Bodman KB, Roitt IM. Changes in normal glycosylation mechanisms in autoimmune rheumatic disease. J Clin Invest (1992) 89(3) 1021-1031. 

Pristane (2,6,10,14-tetramethylpentadecane) is a mineral oil known to induce arthritis, also called pristane-induced arthritis, in an experimental disease model (Wooley Whalen, 1991). Pristane-induced arthritis is MHC-haplotype dependent. DBA/1 mice, but not DBA/2 mice, are susceptible. The disease is accompanied by a broad spectrum of autoantibodies (rheumatoid factor, anticollagen, antibodies to heat shock protein). Pristane-induced arthritis is clearly immune dependent, since it is not observed in nu/nu mice and irradiated mice (Wooley Whalen, 1991). CD4+ T cells and polyclonal T cell activation are involved in the disease process (Wooley et al., 1998), and disease can be prevented by CD4+ Th2 cells specific for 65-kilodalton heat shock protein (Beech et al., 1997). 

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