Immunization with type II collagen (CII), a major constituent of hyaline cartilage, was first demonstrated by Trentham and colleagues in 1977 to be arthritogenic in rats. In the years to follow, CIA has been induced in several animals including mice, goats and rhesus monkeys. One of the hallmark features of CIA is the production of CH-specific antibodies and CH-reactive T cells during the arthritogenic process, as seen in some patients with RA. Furthermore, the histopathological features of CIA resemble RA, with the formation of synovial infiltrates, that lead to pannus formation, marginal bone erosions and joint deformity.
Both humoral and cellular responses have been implicated in the pathogenesis of CIA. Antibodies against CII are detectable 9 days following immunization and an immunoglobulin M (IgM) response peaks within 2 weeks; peak IgG levels are attained at 4-5 weeks postimmunization. Anti-collagen IgG levels coincide with the onset of arthritis, suggesting a role for autoantibodies in the pathogenesis of CIA.
Table 1 Comparison between animal models and RA
Animal species Mice, rats monkeys, goats
Genetic predisposition + Mediators T cells +
Joint involvement Peripheral +
Relapsing/remitting Antigen? Type II
Cell wall arthritis
Mice, rats Mice, rats
Group A Streptococcal cell wall
Rabbits, rats mice, guinea pigs
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