University Library
  • Login
A gateway to Melbourne's research publications
Minerva Access is the University's Institutional Repository. It aims to collect, preserve, and showcase the intellectual output of staff and students of the University of Melbourne for a global audience.
View Item 
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Melbourne Medical School
  • Microbiology & Immunology
  • Microbiology & Immunology - Research Publications
  • View Item
  • Minerva Access
  • Medicine, Dentistry & Health Sciences
  • Melbourne Medical School
  • Microbiology & Immunology
  • Microbiology & Immunology - Research Publications
  • View Item
JavaScript is disabled for your browser. Some features of this site may not work without it.

    A fundamental bimodal role for neuropeptide Y1 receptor in the immune system

    Thumbnail
    Download
    published version (1.483Mb)

    Citations
    Scopus
    Web of Science
    Altmetric
    146
    124
    Author
    Wheway, J; Mackay, CR; Newton, RA; Sainsbury, A; Boey, D; Herzog, H; Mackay, F
    Date
    2005-12-05
    Source Title
    Journal of Experimental Medicine
    Publisher
    ROCKEFELLER UNIV PRESS
    University of Melbourne Author/s
    Mackay, Fabienne
    Affiliation
    Microbiology and Immunology
    Metadata
    Show full item record
    Document Type
    Journal Article
    Citations
    Wheway, J., Mackay, C. R., Newton, R. A., Sainsbury, A., Boey, D., Herzog, H. & Mackay, F. (2005). A fundamental bimodal role for neuropeptide Y1 receptor in the immune system. JOURNAL OF EXPERIMENTAL MEDICINE, 202 (11), pp.1527-1538. https://doi.org/10.1084/jem.20051971.
    Access Status
    Open Access
    URI
    http://hdl.handle.net/11343/257069
    DOI
    10.1084/jem.20051971
    Abstract
    Psychological conditions, including stress, compromise immune defenses. Although this concept is not novel, the molecular mechanism behind it remains unclear. Neuropeptide Y (NPY) in the central nervous system is a major regulator of numerous physiological functions, including stress. Postganglionic sympathetic nerves innervating lymphoid organs release NPY, which together with other peptides activate five Y receptors (Y1, Y2, Y4, Y5, and y(6)). Using Y1-deficient (Y1(-/-)) mice, we showed that Y1(-/-) T cells are hyperresponsive to activation and trigger severe colitis after transfer into lymphopenic mice. Thus, signaling through Y1 receptor on T cells inhibits T cell activation and controls the magnitude of T cell responses. Paradoxically, Y1(-/-) mice were resistant to T helper type 1 (Th1) cell-mediated inflammatory responses and showed reduced levels of the Th1 cell-promoting cytokine interleukin 12 and reduced interferon gamma production. This defect was due to functionally impaired antigen-presenting cells (APCs), and consequently, Y1(-/-) mice had reduced numbers of effector T cells. These results demonstrate a fundamental bimodal role for the Y1 receptor in the immune system, serving as a strong negative regulator on T cells as well as a key activator of APC function. Our findings uncover a sophisticated molecular mechanism regulating immune cell functions that can lead to stress-induced immunosuppression.

    Export Reference in RIS Format     

    Endnote

    • Click on "Export Reference in RIS Format" and choose "open with... Endnote".

    Refworks

    • Click on "Export Reference in RIS Format". Login to Refworks, go to References => Import References


    Collections
    • Minerva Elements Records [45770]
    • Microbiology & Immunology - Research Publications [1555]
    Minerva AccessDepositing Your Work (for University of Melbourne Staff and Students)NewsFAQs

    BrowseCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
    My AccountLoginRegister
    StatisticsMost Popular ItemsStatistics by CountryMost Popular Authors