• Find People
  • Campus Map
  • PiratePort
  • A-Z
    • About
    • Submit
    • Browse
    • Login
    View Item 
    •   ScholarShip Home
    • Health Sciences Campus
    • Brody School of Medicine
    • Microbiology and Immunology
    • View Item
    •   ScholarShip Home
    • Health Sciences Campus
    • Brody School of Medicine
    • Microbiology and Immunology
    • View Item
    JavaScript is disabled for your browser. Some features of this site may not work without it.

    Browse

    All of The ScholarShipCommunities & CollectionsDateAuthorsTitlesSubjectsTypeDate SubmittedThis CollectionDateAuthorsTitlesSubjectsTypeDate Submitted

    My Account

    Login

    Statistics

    View Google Analytics Statistics

    Molecular basis for the immunosuppressive action of stearic acid on T cells.

    Thumbnail
    View/ Open
    Molecular basis immunosuppressive action.pdf (1.052Mb)

    Show full item record
    Author
    Tebbey, P. W.; Buttke, Thomas M.
    Abstract
    Studies were performed to determine the mechanism by which stearic acid (18: 0) selectively inhibits T-dependent immune responses in vitro. Incubation of mitogen-activated B and T cells with 18:0 resulted in dissimilar patterns of incorporation of the saturated fatty acid into their membranes. High-performance liquid chromatography (HPLC) analyses of T cells showed an accumulation of desaturated 18:0-containing phosphatidylcholine (PC) that replaced normal cellular PC. Less significant quantities of the same PC species were seen to accumulate in B-cell membranes; rather, they increased their proportion of oleic acid (18: 1)-containing PC. The different lipid compositions of the lymphocyte cell membranes after exposure to 18:0 were correlated with their plasma membrane potentials. In T cells, the accumulation ofdesaturated, 18: 0-containing PC coincided with a rapid (within 8 hr) collapse ofmembrane integrity, as determined by flow cytometry. The collapse of membrane integrity was found to be time and dose dependent. No such depolarization was observed in B cells which, by virtue of their desaturating ability, were able to avoid incorporating large amounts of desaturated 18: 0-containing phospholipids into their membranes. It is proposed that a lack of stearoyl-CoA desaturase in T cells precludes them from desaturating exogenously derived 18:0, thus leading to increased proportions of 18:0-containing desaturated PC in their cell membranes. The increased abundance of this PC species may enhance membrane rigidity to an extent that plasma membrane integrity is significantly impaired, leading to a loss ofmembrane potential and ultimately cell function and viability. Originally published Immunology, Vol. 70, No. 3, July 1990
    URI
    http://hdl.handle.net/10342/3426
    Subject
     Stearic acid; T-dependent immune response; Response mechanisms 
    Date
    1990-07
    Citation:
    APA:
    Tebbey, P. W., & Buttke, Thomas M.. (July 1990). Molecular basis for the immunosuppressive action of stearic acid on T cells.. Immunology, 70(3), 379- 386. Retrieved from http://hdl.handle.net/10342/3426

    Display/Hide MLA, Chicago and APA citation formats.

    MLA:
    Tebbey, P. W., and Buttke, Thomas M.. "Molecular basis for the immunosuppressive action of stearic acid on T cells.". Immunology. 70:3. (379-386), July 1990. September 22, 2023. http://hdl.handle.net/10342/3426.
    Chicago:
    Tebbey, P. W. and Buttke, Thomas M., "Molecular basis for the immunosuppressive action of stearic acid on T cells.," Immunology 70, no. 3 (July 1990), http://hdl.handle.net/10342/3426 (accessed September 22, 2023).
    AMA:
    Tebbey, P. W., Buttke, Thomas M.. Molecular basis for the immunosuppressive action of stearic acid on T cells.. Immunology. July 1990; 70(3): 379-386. http://hdl.handle.net/10342/3426. Accessed September 22, 2023.
    Collections
    • Microbiology and Immunology
    Publisher
    East Carolina University

    xmlui.ArtifactBrowser.ItemViewer.elsevier_entitlement

    East Carolina University has created ScholarShip, a digital archive for the scholarly output of the ECU community.

    • About
    • Contact Us
    • Send Feedback