Amyloid resistance in A/J mice. Studies with a transfer model

Abstract

Amyloidosis was studied in CBA/J and A/J mice using a classic method of amyloid induction and a transfer model. A/J mice required over 3 times as many injections of azocasein to develop splenic amyloidosis as the CBA/J strain. Perifollicular cellular proliferation occurred after fewer injections in CBA/J mice. In vitro azocasein-stimulated DNA synthetic activity, assayed by incorporation of tritiated thymidine in spleen cell cultures, was greater in CBA/J than A/J mice. Both strains developed amyloidosis after three or four azocasein injections, following sublethal irradiation and intravenous administration of spleen homogenates from azocasein-treated CBA donors. Amyloidosis was accelerated by A/J spleen homogenates only when the donors were given a prolonged course of azocasein. Transfer amyloidosis could be induced in both strains when the irradiation step was eliminated, although the amount of perifollicular amyloid was less. These results demonstrate that the mechanism of amyloid resistance in A/J mice lies in the response to the inducing agent in the preamyloid phase of amyloidogenesis.