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dc.contributor.advisorZaghouani, Habibeng
dc.contributor.authorHoeman, Christineeng
dc.contributor.corporatenameUniversity of Missouri--Columbia. School of Medicineeng
dc.contributor.meetingnameHealth Sciences Research Day (2010 : University of Missouri)eng
dc.date.issued2010eng
dc.description.abstractIt is known that neonates are highly susceptible to microbial infections and allergic reactions. This susceptibility is due to a lack of Th1 cells and an excess of its Th2 counterparts. However, the mechanism underlying this Th1/Th2 imbalance has not been clearly elucidated. Although both Th1 and Th2 cells are present in the primary response, only Th1 cells up-regulate the IL- 13R[alpha]1 chain. Consequently IL-13R[alpha]1 can associate with IL-4R[alpha] to form a heteroreceptor through which IL-4 from Th2 cells can signal and cause the apoptosis of Th1 cells upon secondary re-challenge with antigen. Formation of this IL-13R[alpha]1/IL-4R[alpha] heteroreceptor is influenced by two factors: the neonatal environment and intrinsic T cell factors.eng
dc.format.extent1 pageeng
dc.identifier.urihttp://hdl.handle.net/10355/9205
dc.languageEnglisheng
dc.relation.ispartofcommunityUniversity of Missouri--Columbia. Health Sciences Research Dayeng
dc.rightsOpenAccess.eng
dc.rights.licenseThis work is licensed under a Creative Commons Attribution-NonCommercial-NoDerivs 3.0 License.eng
dc.subjectimmune systemeng
dc.subjectenvironmental factorseng
dc.subject.FASTMaternally acquired immunityeng
dc.subject.FASTNewborn infantseng
dc.subject.FASTT cellseng
dc.titleDon't be such a baby! or the effects of the environment and T cells on neonatal immunity [abstract]eng
dc.typeAbstracteng


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