Abstract
Increased natural killer (NK) cell activity was found in the spleen and peritoneal cavity of mice infected with Babesia microti or Plasmodium vinckei petteri. This increased activity appeared not to be associated with the effectiveness of the host response against these parasites, since it reached its maximum when the parasitaemia was still low, and had decreased by the time the parasites reached peak densities. In addition mice pretreated with 89Strontium or 17β-oestradiol experienced the same pattern of infection as did control mice, yet the infections induced much lower levels of NK activity in the pretreated mice. The course of infection with B. microti was also unaltered in beige mice, which are genetically deficient in NK cells. Thus we consider it unlikely that NK cells are of primary importance in non-specific immunity to these haemoprotozoan infections.