Attenuated immunogenic parasites are essential in the transfer of immunity to virulent Plasmodium berghei.

A less virulent parasite of Plasmodium berghei K173 was isolated that induced immunity against the more virulent parasite. Immunity to this parasite but not to the virulent one, could be transferred by immune spleen cells but not by immune lymph node cells. However, the immune spleen cells did transfer immunity to the virulent strain if accompanied by infection with viable parasites of the less virulent strain, but only if they were allowed to proliferate for a period of 1 week before challenge with the virulent strain. Immune spleen cells could survive two cycles of mouse to mouse transfer. The induction of immunity by transfer of immune spleen cells was associated with the production of anti-parasitic antibody.

The need for live parasites for long-term immunity in malaria.

All of the results of the various experiments support a role for living, proliferating parasites in the efficient induction of anti-parasitic as well as anti-disease (CM) immunity. Non-proliferating parasites or material from disrupted parasites are poor or non-antigens in this respect. Three possibilities as to why living parasites are important in immunity could be considered: 1. circulating parasites contain insufficient antigen to induce protective immunity, but sufficient antigen can be produced during proliferation; 2. only circulating parasites arrive at critical places (e.g. parts of the white pulp of the spleen) for the presentation of the important antigen or induction of appropriate signals. 3. Architectural changes are needed (i.e. formation of barrie-cell-complexes) for the immune response to be effective. The first possibility explains why exoantigens, as well as live, proliferating parasites are efficient inducers of anti-CM immunity. Since these immunizations have no effect on parasitemia, additional/other immune reaction(s) are needed for anti-parasitic immunity. The important role of the spleen in malaria and malaria immunity is well-known. The second possibility includes the idea that live, proliferating parasites circulate through the spleen continuously where unsatisfactory or infected erythrocytes are removed rather than in the liver. Injected killed parasites or material from them when present in the circulation is to a larger extent taken up by the Kupffer cells from the liver rather than the spleen. Presence and uptake of parasites in the spleen may provide the critical confrontation and/or delivery of signals necessary for the development of immunity.(ABSTRACT TRUNCATED AT 250 WORDS)