Rapid parasite multiplication rate, rather than immunosuppression, causes the death of mice infected with virulent Plasmodium yoelii.
Protective immunity against a lethal malaria challenge infection was passively transferred to naive recipient mice with spleen cells from donor mice bearing a lethal infection with the virulent YM strain of Plasmodium yoelii. Successful transfer of protection was contingent upon the elimination of residual, viable parasites from donor spleen cell suspensions prior to the infusion of cells. Passive transfer experiments failed to detect suppressor cells in the spleens of lethally infected mice because unfractionated spleen cells or T-cell-enriched spleen cells from mice infected with P. yoelii YM did not enhance parasitemias upon infusion into mice infected with cross-reactive nonvirulent P. yoelii 17X. We concluded that a form of protective immunity was generated during the course of virulent infection but that its expression was inconsequential because parasite growth apparently exceeded the capacity of the immune system to clear the infection.
D000818:Animals; D007116:Immunization, Passive; D008288:Malaria / Q000276:immunology* / Q000469:parasitology; D051379:Mice; D010961:Plasmodium / Q000254:growth & development* / Q000472:pathogenicity; D013154:Spleen / Q000276:immunology; D050378:T-Lymphocytes, Regulatory / Q000276:immunology*; D014774:Virulence