Clomerulopathy in mice infected with Plasmodium berghei: induction of an autoimmune process.

1. Apparently a living, metabolizing parasite is required to induce the formation of autoantibodies. 2. It seems unlikely that immune complexes of the first type, i.e., positive for plasmodial antigens, are responsible for the induction of autoantibodies, as the transferred malarious plasma (group B) also contained that type of immune complex, but did not induce the formation of the second type of complex. 3. Although a deregulation of the immunocompetent system will occur in animals with a high parasitemia (immunosuppression), the fact that extremely low parasitemia is sufficient to induce antismoothmuscle antibodies suggests that proliferation of "forbidden clones" of self-reactive lymphocytes is not very likely. 4. Antismooth-muscle antibodies are frequently associated with active chronic hepatitis in man. Whether any damage to liver tissue (6) during malaria infection may be responsible for the induction of antismoothmuscle antibodies remains to be investigated. The clinical relevance of these findings is as yet obscure, and one should be careful in comparing these results of the rodent model with the human situation. 5. It remains to be elucidated whether the high level of so-called nonspecific antibodies in acutely infected mice can be explained entirely by the existence of antibodies to parasitic antigens and to host smooth-muscle antigens.