Abstract
This study builds upon the established genetic control of antimalarial immune responses and prior association studies by using a family-based approach, transmission disequilibrium testing, to identify immune response genes that influence antibody responses to Plasmodium falciparum infection in an endemic Tanzanian population. Candidate polymorphisms are within the interleukin-1 (IL-1) gene cluster, the IL-10 promoter, Major histocompatibility complex class II and III, the 5q31-q33 region, and the T-Cell Receptor beta variable region. There was a significant association between the IL1RN alleles and total IgE. Weak evidence for association was present between polymorphisms in the IL10 promoter region and both anti-P falciparum IgE and IgG4 antibodies.
MeSH terms
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Antibodies, Protozoan / biosynthesis*
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Antibodies, Protozoan / genetics
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Antibodies, Protozoan / immunology
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Antibody Formation / genetics
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Endemic Diseases*
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Genes, MHC Class II*
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Genotype
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HLA-D Antigens / genetics
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Haplotypes / genetics
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Humans
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Immunoglobulin E / biosynthesis*
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Immunoglobulin E / genetics
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Immunoglobulin E / immunology
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Immunoglobulin G / biosynthesis*
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Immunoglobulin G / genetics
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Immunoglobulin G / immunology
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Interleukin-1 / genetics
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Interleukin-10 / genetics
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Interleukin-13 / genetics
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Interleukin-4 / genetics
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Malaria, Falciparum / epidemiology
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Malaria, Falciparum / genetics*
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Malaria, Falciparum / immunology
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Minisatellite Repeats
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Polymorphism, Restriction Fragment Length
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Polymorphism, Single Nucleotide
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Promoter Regions, Genetic / genetics
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Receptors, Antigen, T-Cell, alpha-beta / genetics
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Receptors, Interleukin-1 / genetics
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Tanzania / epidemiology
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Th2 Cells / immunology
Substances
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Antibodies, Protozoan
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HLA-D Antigens
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IL10 protein, human
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IL4 protein, human
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Immunoglobulin G
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Interleukin-1
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Interleukin-13
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Receptors, Antigen, T-Cell, alpha-beta
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Receptors, Interleukin-1
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Interleukin-10
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Interleukin-4
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Immunoglobulin E