{"id":{"repo_id":"uiuc","oai_identifier":"oai:www.ideals.illinois.edu:2142/87624"},"canonical_url":"https://search.dev.ndltd.org/etd/uiuc/oai:www.ideals.illinois.edu:2142/87624","repository":{"repo_id":"uiuc","name":"University of Illinois - Urbana-Champaign","base_url":"https://www.ideals.illinois.edu/oai-pmh"},"display":{"title":"Genetic and Sex Steroid Hormone Contributions to the Sexual Dimorphism in Murine Experimental Allergic Encephalomyelitis","abstract":"We found that the composition of the adjuvant used to induce EAE had important implications on the degree of genetic susceptibility necessary to result in disease. We also found that of the many quantitative trait loci (QTL) identified to date, genetic linkages to mouse chromosomes 7 and 11 were strongly associated with susceptibility to EAE. Further, the role of sex steroid hormones and parent-of-origin effects were studied through the use of reciprocal crosses of SJL/J and BI0.S/SgMcdJ mice. We found that adult gonadal hormones selectively regulate sexually dimorphic quantitative traits observed in EAE at the clinical, histopathologic, and genetic levels. Furthermore, we identified specific genetic linkages to chromosomes 3, 4, and 7 which were dependent on the presence or absence of gonadal sex steroids. These findings help explain the important roles of sex steroid hormones in the pathogenesis of EAE. By identifying genetic linkage in the context of specific immunologic and hormonal environments we have begun the process to identify specific genetic-environmental interactions underlying susceptibility to EAE.","abstract_html":"We found that the composition of the adjuvant used to induce EAE had important implications on the degree of genetic susceptibility necessary to result in disease. We also found that of the many quantitative trait loci (QTL) identified to date, genetic linkages to mouse chromosomes 7 and 11 were strongly associated with susceptibility to EAE. Further, the role of sex steroid hormones and parent-of-origin effects were studied through the use of reciprocal crosses of SJL/J and BI0.S/SgMcdJ mice. We found that adult gonadal hormones selectively regulate sexually dimorphic quantitative traits observed in EAE at the clinical, histopathologic, and genetic levels. Furthermore, we identified specific genetic linkages to chromosomes 3, 4, and 7 which were dependent on the presence or absence of gonadal sex steroids. These findings help explain the important roles of sex steroid hormones in the pathogenesis of EAE. By identifying genetic linkage in the context of specific immunologic and hormonal environments we have begun the process to identify specific genetic-environmental interactions underlying susceptibility to EAE.","abstract_has_math":false,"creators":["Fillmore, Parley Dehlin"],"institution":"University of Illinois at Urbana-Champaign","degree_name":"Ph.D.","degree_level":"Dissertation","degree_discipline":"Veterinary Pathobiology","degree_department":null,"school":null,"contributors":["James Zachary"],"advisors":[],"committee_chairs":[],"committee_members":[],"year":2015,"date_issued":"2015-09-28T16:21:37Z","date_published":"2015-09-28T16:21:37Z","updated_at":"2026-07-22T22:26:30Z","subjects":["Biology, Animal Physiology"],"languages":["eng"],"rights":[],"rights_urls":[],"identifier_entries":[{"key":"dc:identifier","label":"Identifier","values":["(MiAaPQ)AAI3130916"],"render_values":[{"text":"(MiAaPQ)AAI3130916","href":null,"code":true}]}]},"links":{"outbound_url":"http://hdl.handle.net/2142/87624","outbound_label":"Handle","outbound_source":"dc:identifier"},"metadata_groups":[{"id":"people","label":"People","entries":[{"key":"dc:contributor","label":"Contributor","values":["James Zachary"]},{"key":"dc:creator","label":"Author","values":["Fillmore, Parley Dehlin"]}]},{"id":"academic_context","label":"Academic Context","entries":[{"key":"dc:date","label":"Dc Date","values":["2015-09-28T16:21:37Z","10000-01-01","2004"]},{"key":"dc:type","label":"Dc Type","values":["text"]},{"key":"thesis:degree_discipline","label":"Discipline","values":["Veterinary Pathobiology"]},{"key":"thesis:degree_level","label":"Degree Level","values":["Dissertation"]},{"key":"thesis:degree_name","label":"Degree Name","values":["Ph.D."]},{"key":"thesis:institution_name","label":"Thesis Institution Name","values":["University of Illinois at Urbana-Champaign"]}]},{"id":"subjects_keywords","label":"Subjects and Keywords","entries":[{"key":"dc:subject","label":"Dc Subject","values":["Biology, Animal Physiology"]}]},{"id":"language_rights","label":"Language and Rights","entries":[{"key":"dc:language","label":"Dc Language","values":["eng"]}]},{"id":"identifiers","label":"Identifiers","entries":[{"key":"dc:identifier","label":"Identifier","values":["http://hdl.handle.net/2142/87624","(MiAaPQ)AAI3130916"]}]},{"id":"additional","label":"Additional Metadata","entries":[{"key":"dc:description","label":"Description","values":["We found that the composition of the adjuvant used to induce EAE had important implications on the degree of genetic susceptibility necessary to result in disease. We also found that of the many quantitative trait loci (QTL) identified to date, genetic linkages to mouse chromosomes 7 and 11 were strongly associated with susceptibility to EAE. Further, the role of sex steroid hormones and parent-of-origin effects were studied through the use of reciprocal crosses of SJL/J and BI0.S/SgMcdJ mice. We found that adult gonadal hormones selectively regulate sexually dimorphic quantitative traits observed in EAE at the clinical, histopathologic, and genetic levels. Furthermore, we identified specific genetic linkages to chromosomes 3, 4, and 7 which were dependent on the presence or absence of gonadal sex steroids. These findings help explain the important roles of sex steroid hormones in the pathogenesis of EAE. 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We also found that of the many quantitative trait loci (QTL) identified to date, genetic linkages to mouse chromosomes 7 and 11 were strongly associated with susceptibility to EAE. Further, the role of sex steroid hormones and parent-of-origin effects were studied through the use of reciprocal crosses of SJL/J and BI0.S/SgMcdJ mice. We found that adult gonadal hormones selectively regulate sexually dimorphic quantitative traits observed in EAE at the clinical, histopathologic, and genetic levels. Furthermore, we identified specific genetic linkages to chromosomes 3, 4, and 7 which were dependent on the presence or absence of gonadal sex steroids. These findings help explain the important roles of sex steroid hormones in the pathogenesis of EAE. 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