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We examined the dynamics of malaria antibody responses of 84 Kenyan infants from birth to 36 months of age by (i) serology, (ii) variant surface antigen (VSA) assay, (iii) growth inhibitory activity (GIA), and (iv) invasion inhibition assays (IIA) specific for merozoite surface protein 1 (MSP1) and sialic acid-dependent invasion pathway. Maternal antibodies in each of these four categories were detected in cord blood and decreased to their lowest level by approximately 6 months of age. Serologic antibodies to 3 preerythrocytic and 10 blood-stage antigens subsequently increased, reaching peak prevalence by 36 months. In contrast, antibodies measured by VSA, GIA, and IIA remained low even up to 36 months. Infants sensitized to\n            <jats:named-content content-type=\"genus-species\">P. falciparum in utero<\/jats:named-content>\n            , defined by cord blood lymphocyte recall responses to malaria antigens, acquired antimalarial antibodies at the same rate as those who were not sensitized\n            <jats:italic>in utero<\/jats:italic>\n            , indicating that fetal exposure to malaria antigens did not affect subsequent infant antimalarial responses. Infants with detectable serologic antibodies at 12 months of age had an increased risk of\n            <jats:named-content content-type=\"genus-species\">P. falciparum<\/jats:named-content>\n            infection during the subsequent 24 months. We conclude that serologic measures of antimalarial antibodies in children 36 months of age or younger represent biomarkers of malaria exposure rather than protection and that functional antibodies develop after 36 months of age in this population.\n          <\/jats:p>","DOI":"10.1128\/cvi.00452-15","type":"journal-article","created":{"date-parts":[[2015,12,13]],"date-time":"2015-12-13T02:11:36Z","timestamp":1449972696000},"page":"104-116","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":24,"title":["Contrasting Patterns of Serologic and Functional Antibody Dynamics to Plasmodium falciparum Antigens in a Kenyan Birth Cohort"],"prefix":"10.1128","volume":"23","author":[{"given":"Arlene E.","family":"Dent","sequence":"first","affiliation":[{"name":"Center for Global Health and Diseases, Case Western Reserve University, Cleveland, Ohio, USA"},{"name":"Department of Pediatrics, Rainbow Babies and Children's Hospital, 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Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Brendan S.","family":"Crabb","sequence":"additional","affiliation":[{"name":"Burnet Institute, Melbourne, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Alan F.","family":"Cowman","sequence":"additional","affiliation":[{"name":"Walter and Eliza Hall Institute of Medical Research, Parkville, Australia"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Toshihiro","family":"Horii","sequence":"additional","affiliation":[{"name":"Department of Molecular Protozoology, Research Institute for Microbial Diseases, Osaka University, Suita, Osaka, Japan"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Eric","family":"Muchiri","sequence":"additional","affiliation":[{"name":"Division of Vector Borne and Neglected Tropical Diseases, Ministry of Public Health and Sanitation, Nairobi, Kenya"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Peter 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