{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,10,4]],"date-time":"2026-10-04T09:00:42Z","timestamp":1791104442823,"version":"4.1.0"},"reference-count":30,"publisher":"American Society for Microbiology","issue":"12","license":[{"start":{"date-parts":[[2012,12,1]],"date-time":"2012-12-01T00:00:00Z","timestamp":1354320000000},"content-version":"tdm","delay-in-days":0,"URL":"https:\/\/journals.asm.org\/non-commercial-tdm-license"}],"content-domain":{"domain":["journals.asm.org"],"crossmark-restriction":true},"short-container-title":["Infect Immun"],"published-print":{"date-parts":[[2012,12]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n          <jats:p>\n            People in regions of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">Schistosoma mansoni<\/jats:named-content>\n            endemicity slowly acquire immunity, but why this takes years to develop is still not clear. It has been associated with increases in parasite-specific IgE, induced, some investigators propose, to antigens exposed during the death of adult worms. These antigens include members of the tegumental-allergen-like protein family (TAL1 to TAL13). Previously, in a group of\n            <jats:named-content xmlns:xlink=\"http:\/\/www.w3.org\/1999\/xlink\" content-type=\"genus-species\" xlink:type=\"simple\">S. mansoni<\/jats:named-content>\n            -infected Ugandan males, we showed that IgE responses to three TALs expressed in worms (TAL1, -3, and -5) became more prevalent with age. Now, in a subcohort we examined associations of these responses with resistance to reinfection and use the data to propose a mechanism for the slow development of immunity. IgE was measured 9 weeks posttreatment and at reinfection at 2 years (\n            <jats:italic>n<\/jats:italic>\n            = 144). An anti-TAL5 IgE (herein referred to as TAL5 IgE) response was associated with reduced reinfection even after adjusting for age using regression analysis (geometric mean odds ratio, 0.24;\n            <jats:italic>P<\/jats:italic>\n            = 0.016). TAL5 IgE responders were a subset of TAL3 IgE responders, themselves a subset of TAL1 responders. TAL3 IgE and TAL5 IgE were highly cross-reactive, with TAL3 the immunizing antigen and TAL5 the cross-reactive antigen. Transcriptional and translational studies show that TAL3 is most abundant in adult worms and that TAL5 is most abundant in infectious larvae. We propose that in chronic schistosomiasis, older individuals have repeatedly experienced IgE antigens exposed when adult worms die (e.g., TAL3) and that this leads to increasing cross-reactivity with antigens of invading larvae (e.g., TAL5). Progressive accumulation of worm\/larvae cross-reactivity could explain the age-dependent immunity observed in areas of endemicity.\n          <\/jats:p>","DOI":"10.1128\/iai.00641-12","type":"journal-article","created":{"date-parts":[[2012,9,25]],"date-time":"2012-09-25T10:25:58Z","timestamp":1348568758000},"page":"4264-4270","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":47,"title":["Progressive Cross-Reactivity in IgE Responses: an Explanation for the Slow Development of Human Immunity to Schistosomiasis?"],"prefix":"10.1128","volume":"80","author":[{"given":"Colin M.","family":"Fitzsimmons","sequence":"first","affiliation":[{"name":"Department of Pathology, University of Cambridge, Cambridge, United Kindgdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Frances M.","family":"Jones","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cambridge, Cambridge, United Kindgdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Angela","family":"Pinot de Moira","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cambridge, Cambridge, United Kindgdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Anna V.","family":"Protasio","sequence":"additional","affiliation":[{"name":"Wellcome Trust Sanger Institute, Wellcome Trust Genome Campus, Hinxton, Cambridge, United Kingdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Jamal","family":"Khalife","sequence":"additional","affiliation":[{"name":"Centre d'Infection et d'Immunit\u00e9 de Lille, Inserm U1019-UMR CNRS 8204, Institut Pasteur de Lille, Lille, France"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Harriet A.","family":"Dickinson","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cambridge, Cambridge, United Kindgdom"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"Edridah M.","family":"Tukahebwa","sequence":"additional","affiliation":[{"name":"Vector Control Division, Ugandan Ministry of Health, Kampala, Uganda"}],"role":[{"vocabulary":"crossref","role":"author"}]},{"given":"David W.","family":"Dunne","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Cambridge, Cambridge, United Kindgdom"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_2_2_2","doi-asserted-by":"publisher","DOI":"10.1186\/1476-7961-5-2"},{"key":"e_1_3_2_3_2","doi-asserted-by":"publisher","DOI":"10.1016\/S0091-6749(96)70306-8"},{"key":"e_1_3_2_4_2","doi-asserted-by":"publisher","DOI":"10.1098\/rspb.2001.1821"},{"key":"e_1_3_2_5_2","doi-asserted-by":"publisher","DOI":"10.1016\/0020-7519(71)90045-2"},{"key":"e_1_3_2_6_2","doi-asserted-by":"publisher","DOI":"10.4269\/ajtmh.1978.27.951"},{"key":"e_1_3_2_7_2","doi-asserted-by":"publisher","DOI":"10.1093\/infdis\/168.4.1000"},{"key":"e_1_3_2_8_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182000066890"},{"key":"e_1_3_2_9_2","doi-asserted-by":"publisher","DOI":"10.1002\/eji.1830220622"},{"key":"e_1_3_2_10_2","doi-asserted-by":"publisher","DOI":"10.1046\/j.1365-3024.1997.d01-186.x"},{"key":"e_1_3_2_11_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pntd.0000543"},{"key":"e_1_3_2_12_2","doi-asserted-by":"publisher","DOI":"10.1371\/journal.pntd.0001593"},{"key":"e_1_3_2_13_2","doi-asserted-by":"publisher","DOI":"10.1159\/000095997"},{"key":"e_1_3_2_14_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182000080896"},{"key":"e_1_3_2_15_2","doi-asserted-by":"publisher","DOI":"10.1017\/S003118200007414X"},{"key":"e_1_3_2_16_2","doi-asserted-by":"publisher","DOI":"10.1038\/349243a0"},{"key":"e_1_3_2_17_2","doi-asserted-by":"publisher","DOI":"10.1016\/0020-7519(73)90004-0"},{"key":"e_1_3_2_18_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0022149X0002664X"},{"key":"e_1_3_2_19_2","doi-asserted-by":"publisher","DOI":"10.1017\/S0031182098003576"},{"key":"e_1_3_2_20_2","doi-asserted-by":"crossref","first-page":"41","DOI":"10.1084\/jem.152.1.41","article-title":"Studies of the antibody-dependent killing of schistosomula of Schistosoma mansoni employing haptenic target antigens. 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