Abstract
Models of rheumatoid arthritis (RA) in laboratory animals are important tools for research into pathogenic mechanisms and the development of effective, safe therapies. Rodent models (rats and mice) have provided important information about the pathogenic mechanisms. However, the evolutionary distance between rodents and humans hampers the translation of scientific principles into effective therapies. The impact of the genetic distance between the species is especially seen with treatments based on biological molecules, which are usually species-specific. The outbred nature and the closer anatomical, genetic, microbiological, physiological, and immunological similarity of nonhuman primates to humans may help to bridge the wide gap between inbred rodent strain models and the heterogeneous RA patient population. Here we review clinical, immunological and pathological aspects of the rhesus monkey model of collagen-induced arthritis, which has emerged as a reproducible model of human RA in nonhuman primates.
Highlights
Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology [1,2]
The ethical management of the rhesus monkey collagen-induced arthritis (CIA) model relies on a semiquantitative clinical scoring system that represents the overall disease status of the animals (Table 2)
A low-molecular-weight CCR5 antagonist that prevents the binding of its ligand, and the migration of these destructive T cells, was tested in the CIA model of rhesus 149
Summary
Rheumatoid arthritis (RA) is a chronic inflammatory disease of unknown etiology [1,2]. The incidence and clinical presentation of collagen-induced arthritis (CIA) in a random sample (more than 50) of the large, outbred rhesus monkey colony at our institute (more than 1,200 animals) appeared heterogeneous, as is observed for human RA. In the CIA model, CRP is elevated before macroscopic clinical signs are observed and can be used as an early marker for disease onset.
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