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Some B-cell deficient mice drug-rescued with clindamycin HCl from otherwise lethal infections with Plasmodium yoelii resisted subsequent challenge with the same parasite despite the fact that they lacked detectable antibody to plasmodia. Parasitemias remained patent but at low levels (
5%) in these mice for prolonged periods of time, suggesting that some T-cell function independent of antibody formation can in part mediate immunity to malaria.
Accepted for publication September 2, 1978.
* This work was supported in part by Public Health Service research grant AI-12710 from the National Institute of Allergy and Infectious Diseases.
Present address: National Center for Toxological Research, Jefferson, Arkansas 72709.
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