{"status":"ok","message-type":"work","message-version":"1.0.0","message":{"indexed":{"date-parts":[[2026,9,21]],"date-time":"2026-09-21T18:31:14Z","timestamp":1790015474476,"version":"4.0.1"},"reference-count":37,"publisher":"American Society for Microbiology","issue":"5","license":[{"start":{"date-parts":[[2003,5,1]],"date-time":"2003-05-01T00:00:00Z","timestamp":1051747200000},"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":[[2003,5]]},"abstract":"<jats:title>ABSTRACT<\/jats:title>\n                  <jats:p>\n                    Primary and secondary murine and human infections with\n                    <jats:italic>Brugia malayi<\/jats:italic>\n                    are characterized by substantial increases in levels of immunoglobulin E (IgE). To investigate whether this is necessary for worm clearance, IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice were subjected to primary- and secondary-infection protocols. Following a primary infection, IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice displayed a profound deficit in their ability to clear an intraperitoneal injection of L3 infective-stage larvae in comparison to wild-type counterparts and maintained substantial worm burdens as late as 10 weeks postinfection. Although viable adult parasites were recovered at this late time point from IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice, the majority of the mice remained free of microfilariae. IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    cohorts subjected to a secondary-infection protocol were able to clear the challenge inoculation in an accelerated manner, with kinetics similar to that observed in the wild-type animals. Analysis of the humoral response in IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice following infection demonstrates a defect in IgG1 and IgG2a production, in addition to the expected lack of IgE. The IgG1 deficiency is no longer evident following a secondary infection. These data imply that deficiencies other than IgE production (i.e., IgG1 production) deficiency may be responsible for the increased permissiveness of IgE\n                    <jats:sup>\u2212\/\u2212<\/jats:sup>\n                    mice as hosts following infection with\n                    <jats:italic>B. malayi<\/jats:italic>\n                    .\n                  <\/jats:p>","DOI":"10.1128\/iai.71.5.2462-2467.2003","type":"journal-article","created":{"date-parts":[[2003,4,18]],"date-time":"2003-04-18T16:54:09Z","timestamp":1050684849000},"page":"2462-2467","update-policy":"https:\/\/doi.org\/10.1128\/asmj-crossmark-policy-page","source":"Crossref","is-referenced-by-count":22,"title":["Mice Genetically Deficient in Immunoglobulin E Are More Permissive Hosts than Wild-Type Mice to a Primary, but Not Secondary, Infection with the Filarial Nematode\n                    <i>Brugia malayi<\/i>"],"prefix":"10.1128","volume":"71","author":[{"given":"L. 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V.","family":"Rajan","sequence":"additional","affiliation":[{"name":"Department of Pathology, University of Connecticut Health Center, Farmington, Connecticut 06030-3105"}],"role":[{"vocabulary":"crossref","role":"author"}]}],"member":"235","reference":[{"key":"e_1_3_1_2_2","doi-asserted-by":"publisher","DOI":"10.1128\/IAI.68.5.3034-3035.2000"},{"key":"e_1_3_1_3_2","doi-asserted-by":"crossref","first-page":"1395","DOI":"10.4049\/jimmunol.150.4.1395","volume":"150","year":"1993","unstructured":"Bancroft, A. J., R. K. Grencis, K. J. Else, and E. Devaney. 1993. Cytokine production in BALB\/c mice immunized with radiation attenuated third stage larvae of the filarial nematode, Brugia pahangi. J. Immunol.150:1395-1402.","journal-title":"J. Immunol."},{"key":"e_1_3_1_4_2","first-page":"143","volume":"23","year":"1984","unstructured":"Butterworth, A. E. 1984. Cell-mediated damage to helminths. Adv. Parasitol.23:143-235.","journal-title":"Adv. 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