Hypergammaglobulinemia in mink was produced by the injection of crude tissue suspensions from mink with spontaneous Aleutian disease. The initiating factor was found to be resistant to 0.3 per cent formalin for 2 weeks but not 40 weeks at 5°C. Foreign antigens as well as formalinized normal mink tissue from homologous and heterologous genotypes did not cause a detectable change in the serum protein values.
Mink homozygous recessive for the Aleutian gene were found to be significantly more susceptible to the experimental disease.
Possible pathogenetic mechanisms as well as similarities between the mink disease and certain immunologic and connective tissue diseases of man are discussed.