ABSTRACT
Reactive systemic amyloidosis is a complication to rheumatoid arthritis and other recurrent inflammatory disorders. Protein AA, an N-terminal cleavage product of the acute phase protein serum amyloid A, forms amyloid fibrils that are deposited in tissue as amyloid aggregates. In an experimental model, resolution of light chain amyloidosis was accelerated, when animals were treated with amyloid-specific antibodies. There is evidence that auto-antibodies directed against protein AA occur in patients with rheumatoid arthritis. Since it is possible to promote amyloid regression by immunological modulation, it is believed that the natural resolution of amyloid that occurs in reactive amyloidosis is mediated by an adaptive immunological mechanism. Reactive amyloidosis was induced in a female out-bred NMRI mouse using silver nitrate and amyloid enhancing factor. Silver nitrate injections were repeated once weekly, six times. After another five months, a silver nitrate booster was given and the animal was killed three days later.
