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Predicate | Object |
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rdf:type | |
lifeskim:mentions | |
pubmed:issue |
12
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pubmed:dateCreated |
1993-2-23
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pubmed:abstractText |
Recent in vitro studies suggest that IgE production in adults is co-ordinately regulated by negative signals from gamma IFN-producing CD4+ T-helper-1 (TH-1) and positive signals from IL-4 producing (TH-2) T-cells. Additionally, seroepidemiological evidence has pinpointed infancy as the period of maximum lifetime risk for T-cell sensitization to ubiquitous environmental antigens. The present study sought to elucidate the relationship between these observations, by examination of CD4+ T-cell function in normal children and those genetically at 'high risk' for atopy, spanning the age range (up to 4 years) in which IgE responses to environmental allergens is typically manifest. Immunocompetent T-cell precursor frequencies (determined by cloning at limiting dilution) were markedly reduced in 'high risk' children relative to normals (0.53 +/- 0.29 vs 0.26 +/- 0.19; P = 0.0025). Consistent with reports from other laboratories employing bulk T-cell culture techniques, the gamma IFN producing capacity of CD4+ T-cell clones from both groups of children were markedly reduced relative to adults, and was lowest in the high risk group (P < 0.02). IL-4 production by CD4+ T-cell clones from the normal children was within the adult range, but again was significantly lower in the high risk group (P < 0.00005). This indicates that initial immune responses to environmental allergens in early childhood occur against a background of maturational 'deficiency' in CD4+ T-cell function, and suggests the possibility that variations in the rate of postnatal maturation of T-cell competence may be a contributing factor in the development of differing patterns of immunological responsiveness to environmental allergens.
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pubmed:language |
eng
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pubmed:journal | |
pubmed:citationSubset |
IM
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pubmed:chemical | |
pubmed:status |
MEDLINE
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pubmed:month |
Dec
|
pubmed:issn |
0954-7894
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pubmed:author | |
pubmed:issnType |
Print
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pubmed:volume |
22
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pubmed:owner |
NLM
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pubmed:authorsComplete |
Y
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pubmed:pagination |
1093-9
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pubmed:dateRevised |
2008-11-21
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pubmed:meshHeading |
pubmed-meshheading:1486538-Adult,
pubmed-meshheading:1486538-Animals,
pubmed-meshheading:1486538-Animals, Newborn,
pubmed-meshheading:1486538-Child, Preschool,
pubmed-meshheading:1486538-Clone Cells,
pubmed-meshheading:1486538-Cytokines,
pubmed-meshheading:1486538-Humans,
pubmed-meshheading:1486538-Hypersensitivity,
pubmed-meshheading:1486538-Immunocompetence,
pubmed-meshheading:1486538-Infant,
pubmed-meshheading:1486538-Interferon-gamma,
pubmed-meshheading:1486538-Interleukin-4,
pubmed-meshheading:1486538-Risk Factors,
pubmed-meshheading:1486538-T-Lymphocytes
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pubmed:year |
1992
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pubmed:articleTitle |
Genetic 'risk' for atopy is associated with delayed postnatal maturation of T-cell competence.
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pubmed:affiliation |
Western Australian Research Institute for Child Health, Subiaco.
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pubmed:publicationType |
Journal Article,
Comparative Study,
Research Support, Non-U.S. Gov't
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