• Login
    JavaScript is disabled for your browser. Some features of this site may not work without it.
    CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes. 
    •   QMRO Home
    • William Harvey Research Institute
    • Centre for Experimental Medicine and Rheumatology (EMR)
    • CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes.
    •   QMRO Home
    • William Harvey Research Institute
    • Centre for Experimental Medicine and Rheumatology (EMR)
    • CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes.
    ‌
    ‌

    Browse

    All of QMROCommunities & CollectionsBy Issue DateAuthorsTitlesSubjectsThis CollectionBy Issue DateAuthorsTitlesSubjects
    ‌
    ‌

    Administrators only

    Login
    ‌
    ‌

    Statistics

    Most Popular ItemsStatistics by CountryMost Popular Authors

    CD5 expression promotes IL-10 production through activation of the MAPK/Erk pathway and upregulation of TRPC1 channels in B lymphocytes.

    View/Open
    Published version
    Embargoed until: 5555-01-01
    Reason: Publisher version
    Accepted version (1.285Mb)
    Volume
    15
    Pagination
    158 - 170
    DOI
    10.1038/cmi.2016.42
    Journal
    Cell Mol Immunol
    Issue
    2
    Metadata
    Show full item record
    Abstract
    CD5 is constitutively expressed on T cells and a subset of mature normal and leukemic B cells in patients with chronic lymphocytic leukemia (CLL). Important functional properties are associated with CD5 expression in B cells, including signal transducer and activator of transcription 3 activation, IL-10 production and the promotion of B-lymphocyte survival and transformation. However, the pathway(s) by which CD5 influences the biology of B cells and its dependence on B-cell receptor (BCR) co-signaling remain unknown. In this study, we show that CD5 expression activates a number of important signaling pathways, including Erk1/2, leading to IL-10 production through a novel pathway independent of BCR engagement. This pathway is dependent on extracellular calcium (Ca2+) entry facilitated by upregulation of the transient receptor potential channel 1 (TRPC1) protein. We also show that Erk1/2 activation in a subgroup of CLL patients is associated with TRPC1 overexpression. In this subgroup of CLL patients, small inhibitory RNA (siRNA) for CD5 reduces TRPC1 expression. Furthermore, siRNAs for CD5 or for TRPC1 inhibit IL-10 production. These findings provide new insights into the role of CD5 in B-cell biology in health and disease and could pave the way for new treatment strategies for patients with B-CLL.
    Authors
    Garaud, S; Taher, TE; Debant, M; Burgos, M; Melayah, S; Berthou, C; Parikh, K; Pers, J-O; Luque-Paz, D; Chiocchia, G
    URI
    http://qmro.qmul.ac.uk/xmlui/handle/123456789/15040
    Collections
    • Centre for Experimental Medicine and Rheumatology (EMR) [388]
    Language
    eng
    Licence information
    Original publication is available at http://www.nature.com/cmi/journal/vaop/ncurrent/full/cmi201642a.html
    Copyright statements
    © 2016 Chinese Society of Immunology and The University of Science and Technology of China
    Twitter iconFollow QMUL on Twitter
    Twitter iconFollow QM Research
    Online on twitter
    Facebook iconLike us on Facebook
    • Site Map
    • Privacy and cookies
    • Disclaimer
    • Accessibility
    • Contacts
    • Intranet
    • Current students

    Modern Slavery Statement

    Queen Mary University of London
    Mile End Road
    London E1 4NS
    Tel: +44 (0)20 7882 5555

    © Queen Mary University of London.