Amyloidosis was induced by repeated casein injections in a strain of mice with congenital aplasia of the thymus (nu/nu-C3H). The development of amyloidosis in this strain was delayed compared with the development of amyloidosis in the strain of control mice C3H. Spleen grafts from casein sensitized non-amyloidotic “nude” and C3H mice were transferred to mice from both strains. Only grafts from casein-sensitized C3H mice could accelerate amyloid formation in recipients, whereas grafts from the casein-sensitized “nude” mice had no such effect. Antibodies to casein could be detected neither in the donor mice nor in the recipients. The observed acceleration could be due to a transfer of casein stimulated T-lymphocytes. Spleen cells from amyloidotic “nude” and C3H mice were transferred to both strains. Amyloid formation occurred only in recipients belonging to the C3H strain. As amyloid formation in the recipients—in this transfer model—is dependent on heavy cytotoxic treatment, it seems unlikely that amyloid formation in the recipients is due to immune reactions elicited by donor or recipient lymphoid cells. The reason why amyloidosis cannot be transferred by spleen cells to nude mice could be due to a poorer trapping of donor spleen cells in the nude spleens than in the normal C3H spleens.