• Login
    View Item 
    •   Home
    • UA Graduate and Undergraduate Research
    • UA Theses and Dissertations
    • Dissertations
    • View Item
    •   Home
    • UA Graduate and Undergraduate Research
    • UA Theses and Dissertations
    • Dissertations
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of UA Campus RepositoryCommunitiesTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournalThis CollectionTitleAuthorsIssue DateSubmit DateSubjectsPublisherJournal

    My Account

    LoginRegister

    About

    AboutUA Faculty PublicationsUA DissertationsUA Master's ThesesUA Honors ThesesUA PressUA YearbooksUA CatalogsUA Libraries

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    Regulation of interferon-gamma production in human peripheral blood mononuclear cells: Heredity, relation to markers of allergy and possible role of inducible T cell kinase (ITK)

    • CSV
    • RefMan
    • EndNote
    • BibTex
    • RefWorks
    Thumbnail
    Name:
    azu_td_9992109_sip1_m.pdf
    Size:
    2.767Mb
    Format:
    PDF
    Download
    Author
    Raman, Kavita
    Issue Date
    2000
    Keywords
    Health Sciences, Immunology.
    Advisor
    Halonen, Marilyn
    
    Metadata
    Show full item record
    Publisher
    The University of Arizona.
    Rights
    Copyright © is held by the author. Digital access to this material is made possible by the University Libraries, University of Arizona. Further transmission, reproduction or presentation (such as public display or performance) of protected items is prohibited except with permission of the author.
    Abstract
    IFN-γ and IL-4 are cytokines that are thought to be products of distinct differentiation pathways for lymphocytes and that inhibit and enhance the development of IgE antibodies, respectively. We hypothesized that the level of IFN-γ production upon stimulation of immune cells in the blood is a stable, heritable phenotype that is inversely related to phenotypic markers of allergy and to the Th2 cytokine IL-4. The studies were performed with samples of human blood obtained from children enrolled at birth in a large, longitudinal study of allergy known as the Tucson CRS. Mitogen-stimulated IFN-γ production by PBMCs of children at age 11 was compared to IFN-γ production in the first year of life and found to show a significant positive correlation. The expected inverse relation to markers of allergy (total serum IgE, skin test reactivity and eosinophils) was not observed. A strong positive relation was observed between IFN-γ production in the parents and children, lending support to the concept of genetic regulation. In contrast to the inverse relation hypothesized to IL-4, a positive relation was observed to IL-4 as well as to another cytokine, IL-2. A linkage analysis performed by a colleague showed linkage between low production of IFN-γ and a region of chromosome 5q in which the gene for a T-cell specific kinase (Itk) is located. These results led us to hypothesize a common "regulator" of cytokines that was functioning and might be Itk. Decreased expression and/or decreased function of Itk could account for the low cytokine data. In order to test this hypothesis, ten adult volunteers with low and ten with high cytokine production matched for age and sex were tested for Itk function and expression. The two groups were examined for Itk expression (normalized to CD3 expression) by western blotting. The group of low cytokine producing individuals showed significantly less Itk expression than the high cytokine-producing group. Attempts to optimize an in vitro kinase assay to determine Itk function were unsuccessful. In the absence of functional studies to support the results from the expression studies, it is not possible to say with certainty that Itk function is related to cytokine production. Therefore, we conclude that IFN-γ expression in humans is a stable phenotype with evidence of a genetic basis for regulation and that Itk is a candidate gene contributing to that genetic basis.
    Type
    text
    Dissertation-Reproduction (electronic)
    Degree Name
    Ph.D.
    Degree Level
    doctoral
    Degree Program
    Graduate College
    Microbiology and Immunology
    Degree Grantor
    University of Arizona
    Collections
    Dissertations

    entitlement

     
    The University of Arizona Libraries | 1510 E. University Blvd. | Tucson, AZ 85721-0055
    Tel 520-621-6442 | repository@u.library.arizona.edu
    DSpace software copyright © 2002-2017  DuraSpace
    Quick Guide | Contact Us | Send Feedback
    Open Repository is a service operated by 
    Atmire NV
     

    Export search results

    The export option will allow you to export the current search results of the entered query to a file. Different formats are available for download. To export the items, click on the button corresponding with the preferred download format.

    By default, clicking on the export buttons will result in a download of the allowed maximum amount of items.

    To select a subset of the search results, click "Selective Export" button and make a selection of the items you want to export. The amount of items that can be exported at once is similarly restricted as the full export.

    After making a selection, click one of the export format buttons. The amount of items that will be exported is indicated in the bubble next to export format.