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*
Department of Microbiology and Immunology, Allegheny University of the Health Sciences, Philadelphia, PA 19129; and
Laboratory of Molecular Genetics and Immunology, The Rockefeller University, New York, NY 10021
The mechanisms by which Abs mediate protection during blood-stage
malaria infections is controversial, with some evidence pointing to the
direct effect of Abs on parasite invasion and growth, while other
studies suggest that Abs act in cooperation with monocytes to achieve
parasite inhibition. To determine whether the effector phase of
protection in vivo to the rodent parasite Plasmodium yoelii
yoelii requires Fc receptor bearing cells, we passively
transferred immune sera into FcR 
-chain knockout mice. Inflammatory
macrophages from these knockout mice were unable to mediate
phagocytosis or Ab-dependent cell-mediated cytotoxicity (ADCC) through
FcRI, FcRII, or FcRIII. Passive transfer of either P.
y. yoelii hyperimmune sera or anti-GST-PYC2 sera directed
to the major merozoite surface protein (MSP-1) of this parasite enabled
both BALB/cByJ mice and FcR -chain-deficient mice to resist lethal
P. y. yoelii 17XL (Py17XL) challenge. mAb302, a
protective IgG3 Ab, also passively protected both strains of mice. Most
of these samples contain Ab isotypes that would not be able to protect
mice if their protective effects required Ab-dependent cell-mediated
cytotoxicity. These results establish that, in this infection,
protection is directly mediated by Abs and does not require the
participation of Fc receptors.
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