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*
Department of Allergology and
Center for Experimental Medicine, Institute of Medical Science, University of Tokyo, Tokyo, Japan;
Hijirigaoka Hospital, Tokyo, Japan;
Gunma Prefectural College of Health Science, Maebashi, Japan;
¶
Department of Experimental Immunology, Institute of Development, Aging and Cancer, Tohoku University, Sendai, Japan and Core Research for Evolutional Science and Technology, Japan Science and Technology Corporation, Tokyo, Japan;
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Institute of Experimental Animals, Shinshu University School of Medicine, Matsumoto, Japan;
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Department of Immunology and
**
Intractable Disease Research Center, Tokyo Medical University, Tokyo, Japan; and
The Ogata Institute for Medical & Chemical Research, Tokyo, Japan
Plasmodium berghei XAT is an
irradiation-induced attenuated variant derived from the lethal strain
P. berghei NK65, and its blood-stage parasites are
spontaneously cleared in immune competent mice. In the present study,
we studied the mechanism of host resistance to blood-stage malaria
infection using P. berghei XAT. Infection enhanced
Ab-dependent phagocytosis of PRBC by splenic macrophages in wild-type
C57BL/6 mice. In contrast, FcR 
-chain knockout
(FcR-/-) mice, which lack the ability to mediate
Ab-dependent phagocytosis and Ab-dependent cell-mediated cytotoxicity
through FcRI, FcRII, and FcRIII, could not induce Ab-dependent
phagocytic activity. These FcR-/- mice showed
increased susceptibility to the P. berghei XAT
infection, with eventually fatal results, although they produced
comparable amounts of IFN- by spleen cells and anti-XAT Abs in
serum. In addition, passive transfer of anti-XAT IgG obtained from
wild-type mice that had recovered from infection into
FcR-/- mice could not suppress the increase in
parasitemia, and almost all of these mice died after marked
parasitemia. In contrast, passive transfer of anti-XAT IgG into
control wild-type mice inhibited the increase in parasitemia.
IFN--/- mice, which were highly susceptible to the
P. berghei XAT infection, failed to induce Ab-dependent
phagocytic activity and also showed reduced production of serum
anti-XAT IgG2a isotype compared with control wild-type mice. These
results suggest that FcR-mediated Ab-dependent phagocytosis, which is
located downstream of IFN- production, is important as an effector
mechanism to eliminate PRBC in blood-stage P. berghei
XAT infection.
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