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*
Division of Geographic Medicine, Department of Medicine, Case Western Reserve University and University Hospitals of Cleveland, Cleveland, OH 44106;
Veteran’s Affairs Medical Center, Cleveland, OH 44106;
Kenya Medical Research Institute, Nairobi, Kenya;
Division of Vector Borne Disease, Ministry of Health, Nairobi, Kenya; and
¶ Department of Clinical Pathology, Assuit University, Assuit, Egypt
Infants born in areas of stable malaria transmission are relatively
protected against severe morbidity and high density Plasmodium
falciparum blood-stage infection. This protection may involve
prenatal sensitization and immunologic reactivity to malaria surface
ligands that participate in invasion of red cells. We examined cord
blood T and B cell immunity to P. falciparum merozoite
surface protein-1 (MSP-1) in infants born in an area of stable malaria
transmission in Kenya. T cell cytokine responses to the C-terminal
19-kDa fragment of MSP-1 (MSP-119) were detected in 24 of
92 (26%) newborns (4–192 IFN-
and 3–88 IL-4-secreting cells per
106/cord blood lymphocytes). Peptide epitopes in the
N-terminal block 3 region of MSP-1 also drove IFN- and/or IL-13
production. There was no evidence of prenatal T cell sensitization to
liver-stage Ag-1. A total of 5 of 86 (6%) newborns had cord blood
anti-MSP-119 IgM Abs, an Ig isotype that does not cross
the placenta and is therefore of fetal origin. The frequency of
neonatal B cell sensitization was higher than that indicated by
serology alone, as 5 of 27 (18%) cord blood samples contained B cells
that produced IgG when stimulated with MSP-119 in vitro.
Neonatal B cell IgG responses were restricted to the Q-KNG allele of
MSP-119, the major variant in this endemic area, whereas T
cells responded to all four MSP-119 alleles evaluated. In
utero sensitization to MSP-1 correlated with the presence of malaria
parasites in cord blood (
2 = 20,
p < 0.0001). These data indicate that prenatal
sensitization to blood-stage Ags occurs in infants born in malaria
endemic areas.
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