Relationships between maternal malaria and malarial immune responses in mothers and neonates

Rasheed, F.N.; Bulmer, Judith N.; Andrés, Felipe; Jawla, Muhammed; Jakobsen, Palle; Jepson, Annette; Greenwood, Brian

doi:10.1111/j.1365-3024.1995.tb00960.x

Cited by 62 publications

(55 citation statements)

References 34 publications

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“…[34][35][36][37] Although this study was not able to identify the major factor that leads to the susceptibility to the first malaria infection, the relationship between longer time to the first malaria infection and subsequent lymphocyte proliferation we observed may reflect the overall good status of cellular immunity.…”

Section: Discussionmentioning

confidence: 74%

ASSOCIATION OF INTERFERON-γ RESPONSES TO PRE-ERYTHROCYTIC STAGE VACCINE CANDIDATE ANTIGENS OF PLASMODIUM FALCIPARUM IN YOUNG KENYAN CHILDREN WITH IMPROVED HEMOGLOBIN LEVELS: XV. ASEMBO BAY COHORT PROJECT

et al. 2003

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Abstract. Previous studies in animal models have revealed an association between interferon-␥ (IFN-␥), produced by CD8 + T cells and irradiated sporozoite-induced sterile immunity. To determine whether IFN-␥ can serve as a marker of pre-erythrocytic protective immunity in individuals naturally exposed to malaria, we characterized IFN-␥ and lymphocyte proliferative responses to previously defined CD8 + cytotoxic T lymphocyte (CTL) epitopes from six preerythrocytic stage antigens in 107 children six months to two years old from a community-based birth cohort in western Kenya. We found that IFN-␥ positive responders had higher hemoglobin (Hb) levels and significantly reduced prevalence of severe malarial anemia one month after the test compared with IFN-␥ non-responders, suggesting that IFN-␥ immune responses to these pre-erythrocytic antigens were associated with protection against malarial anemia. Children who responded by lymphocyte proliferation had a significantly longer time to first documented malaria parasitemia after birth; however, there was no correlation between the presence of lymphocyte proliferative response and higher Hb levels. We propose that IFN-␥ production could be used as a potential marker of protective immunity against malaria associated anemia in young children living in malaria holoendemic areas.

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Section: Discussionmentioning

confidence: 74%

ASSOCIATION OF INTERFERON-γ RESPONSES TO PRE-ERYTHROCYTIC STAGE VACCINE CANDIDATE ANTIGENS OF PLASMODIUM FALCIPARUM IN YOUNG KENYAN CHILDREN WITH IMPROVED HEMOGLOBIN LEVELS: XV. ASEMBO BAY COHORT PROJECT

et al. 2003

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“…Study of analogous responses in humans is logistically challenging and limited to examination of humoral and cellular immune responses in cord blood, which reflects the pool of circulating fetal lymphocytes at birth. The presence of IgM or IgE Abs to malaria Ags in cord blood constitutes prima facie evidence of in utero sensitization since, unlike IgG, these Ig isotypes do not cross the placenta from the maternal circulation (8,11,12). There have been relatively fewer studies of cord blood T cell responses to malaria Ags (12)(13)(14) and to our knowledge, no descriptions of cord blood B cell responses.…”

Section: P Regnancy Is Associated With An Increased Risk Of Maternalmentioning

confidence: 99%

Acquired Immune Responses to Plasmodium falciparum Merozoite Surface Protein-1 in the Human Fetus

King

Malhotra

Wamachi

et al. 2002

The Journal of Immunology

104

108

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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-γ 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-γ 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 (χ2 = 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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“…These have demonstrated low level reactivity to schizont extract, and certain blood stage Ag, and lack of reactivity to liver stage Ag [7][8][9][10][11]. Healthy adults living in malaria endemic regions generally have low level cellular reactivity to P. falciparum Ag despite lifelong exposure to parasites [12][13][14].…”

Section: Introductionmentioning

confidence: 99%

The effect of placental malaria infection on cord blood and maternal immunoregulatory responses at birth

et al. 2010

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Placental malaria (PM), a frequent infection of pregnancy, provides an ideal opportunity to investigate the impact on immune development of exposure of the foetal immune system to foreign Ag. We investigated the effect of PM on the regulatory phenotype and function of cord blood cells from healthy Gambian newborns and peripheral blood cells from their mothers, and analyzed for effects on the balance between regulatory and effector responses. Using the gold standard for classifying PM we further distinguished between resolved infection and acute or chronic PM active at the time of delivery. We show that exposure to malarial Ag in utero results in the expansion of malaria-specific FOXP31 Treg and more generalized FOXP3 1 CD4 1 Treg in chronic and resolved PM, alongside increased Th1 pro-inflammatory responses (IFN-c, TNF-a, IFN-c:IL-10) in resolved PM infection only. These observations demonstrate a clear effect of exposure to malarial Ag in foetal life on the immune environment at birth, with a regulatory response dominating in the newborns with ongoing chronic PM, while those with resolved infection produce both regulatory and inflammatory responses. The findings might explain some of the adverse effects on the health of babies born to women with PM.

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Relationships between maternal malaria and malarial immune responses in mothers and neonates

Cited by 62 publications

References 34 publications

ASSOCIATION OF INTERFERON-γ RESPONSES TO PRE-ERYTHROCYTIC STAGE VACCINE CANDIDATE ANTIGENS OF PLASMODIUM FALCIPARUM IN YOUNG KENYAN CHILDREN WITH IMPROVED HEMOGLOBIN LEVELS: XV. ASEMBO BAY COHORT PROJECT

ASSOCIATION OF INTERFERON-γ RESPONSES TO PRE-ERYTHROCYTIC STAGE VACCINE CANDIDATE ANTIGENS OF PLASMODIUM FALCIPARUM IN YOUNG KENYAN CHILDREN WITH IMPROVED HEMOGLOBIN LEVELS: XV. ASEMBO BAY COHORT PROJECT

Acquired Immune Responses to Plasmodium falciparum Merozoite Surface Protein-1 in the Human Fetus

The effect of placental malaria infection on cord blood and maternal immunoregulatory responses at birth

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