Monoclonal antibodies (mAb) have been raised against Plasmodium falciparum gametocyte stage protein extracts, in an effort to identify novel parasite antigens that might mediate malaria transmission-blocking immunity. mAb 1A1 identified Pfs2400, a sexual stage-specific antigen of greater than 2 megadaltons, that is associated with the outer leaflet of the parasitophorous vacuole membrane in mature circulating gametocyte-infected red blood cells. Upon induction of gametogenesis, Pfs2400 partitions between the gamete plasmalemma and the degenerating erythrocyte membrane. The antigen is no longer detectable in the fully emerged gamete. mAb 1A1 dramatically reduces the number of oocysts formed in P. falciparum gametocyte-fed mosquitoes. The cognate antigen is probably the product of the Pf11.1 gene (Scherf et al. 1988. EMBO [Eur. Mol. Biol. Organ.]J. 7:1129) on the basis that a peptide composed of two copies of the degenerate nine amino acid repeat sequence in the Pf11.1 protein, can inhibit binding of mAb1A1 to the native antigen. The mechanism of transmission inhibition mediated by the Pfs2400 is discussed.
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1 February 1993
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February 01 1993
Pfs2400 can mediate antibody-dependent malaria transmission inhibition and may be the Plasmodium falciparum 11.1 gene product.
Z Feng,
Z Feng
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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R N Hoffmann,
R N Hoffmann
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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R S Nussenzweig,
R S Nussenzweig
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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M Tsuji,
M Tsuji
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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H Fujioka,
H Fujioka
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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M Aikawa,
M Aikawa
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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T H Lensen,
T H Lensen
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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T Ponnudurai,
T Ponnudurai
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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L G Pologe
L G Pologe
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
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Z Feng
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
R N Hoffmann
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
R S Nussenzweig
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
M Tsuji
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
H Fujioka
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
M Aikawa
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
T H Lensen
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
T Ponnudurai
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
L G Pologe
Department of Medical and Molecular Parasitology, New York University School of Medicine, New York 10010.
Online ISSN: 1540-9538
Print ISSN: 0022-1007
J Exp Med (1993) 177 (2): 273–281.
Citation
Z Feng, R N Hoffmann, R S Nussenzweig, M Tsuji, H Fujioka, M Aikawa, T H Lensen, T Ponnudurai, L G Pologe; Pfs2400 can mediate antibody-dependent malaria transmission inhibition and may be the Plasmodium falciparum 11.1 gene product.. J Exp Med 1 February 1993; 177 (2): 273–281. doi: https://doi.org/10.1084/jem.177.2.273
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