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    CD11b regulates the Treg/Th17 balance in murine arthritis via IL-6

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    Author
    Stevanin, M.
    Busso, N.
    Chobaz, V.
    Date
    2017
    Journal
    European Journal of Immunology
    Publisher
    Wiley-VCH Verlag
    Type
    Article
    
    Metadata
    Show full item record
    See at
    https://www.doi.org/10.1002/eji.201646565
    Abstract
    Th17 cells are often associated with autoimmunity and been shown to be increased in CD11b−/− mice. Here, we examined the role of CD11b in murine collagen‐induced arthritis (CIA). C57BL/6 and CD11b−/− resistant mice were immunized with type II collagen. CD11b−/− mice developed arthritis with early onset, high incidence, and sustained severity compared with C57BL/6 mice. We observed a marked leukocyte infiltration, and histological examinations of the arthritic paws from CD11b−/− mice revealed that the cartilage was destroyed in association with strong lymphocytic infiltration. The CD11b deficiency led to enhanced Th17‐cell differentiation. CD11b−/− dendritic cells (DCs) induced much stronger IL‐6 production and hence Th17‐cell differentiation than wild‐type DCs. Treatment of CD11b−/− mice after establishment of the Treg/Th17 balance with an anti‐IL‐6 receptor mAb significantly suppressed the induction of Th17 cells and reduced arthritis severity. Finally, the severe phenotype of arthritis in CD11b−/− mice was rescued by adoptive transfer of CD11b+ DCs. Taken together, our results indicate that the resistance to CIA in C57BL/6 mice is regulated by CD11b via suppression of IL‐6 production leading to reduced Th17‐cell differentiation. Therefore, CD11b may represent a susceptibility factor for autoimmunity and could be a target for future therapy. Copyright 2017 WILEY-VCH Verlag GmbH & Co. KGaA, Weinheim
    Sponsors
    The work was supported by grants from the Swiss National Science Foundation to HAO.
    Keyword
    Arthritis
    Autoimmunity
    CD11b integrin
    Dendritic cells
    Th17
    Identifier to cite or link to this item
    https://www.scopus.com/inward/record.uri?eid=2-s2.0-85015196794&doi=10.1002%2feji.201646565&partnerID=40&md5=5b2a0d6c789dce827d7b3deb723608ff; http://hdl.handle.net/10713/10031
    ae974a485f413a2113503eed53cd6c53
    10.1002/eji.201646565
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    UMB Open Access Articles 2017

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