[-] Show simple item record

dc.contributor.advisorZaghouani, Habibeng
dc.contributor.authorHardaway, John C., 1978-eng
dc.date.issued2009eng
dc.date.submitted2009 Summereng
dc.descriptionThesis advisor: Habib Zaghouani.eng
dc.descriptionTitle from PDF of title page (University of Missouri--Columbia, viewed on January 5, 2010).eng
dc.descriptionThe entire dissertation/thesis text is included in the research.pdf file; the official abstract appears in the short.pdf file (which also appears in the research.pdf); a non-technical general description, or public abstract, appears in the public.pdf file.eng
dc.descriptionVita.eng
dc.descriptionPh. D. University of Missouri-Columbia 2009.eng
dc.description.abstract[ACCESS RESTRICTED TO THE UNIVERSITY OF MISSOURI AT REQUEST OF AUTHOR.] Recent work in our lab has demonstrated a role for interleukin-13 receptor alpha 1 (IL-13R[alpha]1) in the induction of apoptosis of T helper type 1 (Th1) cells in the neonatal immune system. Apoptosis of Th1 cells results in neonatal Th2-bias, which confers susceptibility to both microbial infections and allergic reactions. Unfortunately, there have been few molecular tools developed to study IL-13R[alpha]1 in the mouse despite these findings. Therefore, in order to further examine the role of IL-13R[alpha]1 in neonatal immunity, and also in allergy and asthma, we developed a monoclonal antibody that detects IL-13R[alpha]1 and we have generated mice that deficient in the expression of IL-13R[alpha]1. Using these reagents, IL-13R[alpha]1 was found to influence the primary T helper cell response to antigen, which expands upon it's role, since the role of IL-13R[alpha]1 in apoptosis of neonatal Th1 cells was previously observed upon secondary encounter with antigen. Furthermore, we demonstrate that when IL-13R[alhpa]1 deficient T cells are transferred to wild-type BALB/c mice, neonatal Th2-bias is effectively reversed to yield a Th1-dominated response. These observations strengthen IL-13R[alpha]1's candidacy as a molecular target in neonatal vaccines and also in therapies to prevent the formation of allergies.eng
dc.description.bibrefIncludes bibliographical referenceseng
dc.identifier.merlinb73326240eng
dc.identifier.oclc496011044eng
dc.identifier.urihttps://doi.org/10.32469/10355/6977eng
dc.identifier.urihttps://hdl.handle.net/10355/6977
dc.languageEnglisheng
dc.publisherUniversity of Missouri--Columbiaeng
dc.relation.ispartofcollectionUniversity of Missouri--Columbia. Graduate School. Theses and Dissertations.eng
dc.rightsAccess is limited to the campuses of the University of Missouri.eng
dc.subject.lcshImmunityeng
dc.subject.lcshInterleukin-13eng
dc.subject.lcshTh1 cellseng
dc.subject.meshImmunity -- immunologyeng
dc.subject.meshMice, Inbred BALB Ceng
dc.subject.meshTh1 Cells -- immunologyeng
dc.subject.meshInterleukin-13 Receptor Alpha1 Subunit -- immunologyeng
dc.titleExamination of neonatal immunity in IL-13 receptor alpha 1 deficient miceeng
dc.typeThesiseng
thesis.degree.disciplineMicrobiology (Medicine) (MU)eng
thesis.degree.grantorUniversity of Missouri--Columbiaeng
thesis.degree.levelDoctoraleng
thesis.degree.namePh. D.eng


Files in this item

[PDF]
[PDF]
[PDF]

This item appears in the following Collection(s)

[-] Show simple item record