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    Regulation of T cell afferent lymphatic migration by targeting LTβR-mediated non-classical NFκB signaling

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    Author
    Piao, W.
    Xiong, Y.
    Famulski, K.
    Date
    2018
    Journal
    Nature Communications
    Publisher
    Nature Publishing Group
    Type
    Article
    
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    Other Titles
    Regulation of T cell afferent lymphatic migration by targeting lymphotoxin-beta receptor-mediated non-classical NFκB signaling
    See at
    https://dx.doi.org/10.1038/s41467-018-05412-0
    https://www.doi.org/10.1038/s41467-019-10952-0
    Abstract
    Lymphotoxin-beta receptor (LTβR) signaling in lymphatic endothelial cells (LEC) regulates leukocyte afferent lymphatic transendothelial migration (TEM). The function of individual signaling pathways for different leukocyte subsets is currently unknown. Here, we show that LTβR signals predominantly via the constitutive and ligand-driven non-classical NIK pathway. Targeting LTβR-NIK by an LTβR-derived decoy peptide (nciLT) suppresses the production of chemokines CCL21 and CXCL12, and enhances the expression of classical NFκB-driven VCAM-1 and integrin β4 to retain T cells on LEC and precludes T cell and dendritic cell TEM. nciLT inhibits contact hypersensitivity (CHS) at both the sensitization and elicitation stages, likely by inhibiting leukocyte migration. By contrast, targeting LTβR-classical NFκB signaling during the elicitation and resolution stages attenuates CHS, possibly by promoting leukocyte egress. These findings demonstrate the importance of LTβR signaling in leukocyte migration and LEC and lymphatic vessel function, and show that antagonist peptides may serve as lead compounds for therapeutic applications. Copyright 2018, The Author(s).
    Description
    Author Correction for this article is at https://www.doi.org/10.1038/s41467-019-10952-0.
    Keyword
    Endothelial Cells
    Lymphatic Vessels
    Lymphotoxin beta Receptor
    Signal Transduction
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85050989714&doi=10.1038%2fs41467-018-05412-0&partnerID=40&md5=33b5cde07b4d709dd9c52f49982874f1; http://hdl.handle.net/10713/9451
    ae974a485f413a2113503eed53cd6c53
    10.1038/s41467-018-05412-0
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    UMB Open Access Articles 2018

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