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    DOCK8 functions as an adaptor that links TLR-MyD88 signaling to B cell activation

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    Authors
    Jabara, Haifa H.
    McDonald, Douglas R.
    Janssen, Erin
    Massaad, Michel J.
    Ramesh, Narayanaswamy
    Borzutzky, Arturo
    Rauter, Ingrid
    Benson, Halli
    Schneider, Lynda
    Baxi, Sachin
    Recher, Mike
    Notarangelo, Luigi D.
    Wakim, Rima
    Dbaibo, Ghassan
    Dasouki, Majed
    Al-Herz, Waleed
    Barlan, Isil
    Baris, Safa
    Kutukculer, Necil
    Ochs, Hans D.
    Plebani, Alessandro
    Kanariou, Maria
    Lefranc, Gerard
    Reisli, Ismail
    Fitzgerald, Katherine A.
    Golenbock, Douglas T.
    Manis, John
    Keles, Sevgi
    Ceja, Reuben
    Chatila, Talal A.
    Geha, Raif S.
    Show allShow less
    UMass Chan Affiliations
    Department of Medicine, Division of Infectious Diseases and Immunology
    Document Type
    Journal Article
    Publication Date
    2012-05-13
    Keywords
    Adolescent
    Animals
    B-Lymphocytes
    Cell Differentiation
    Child
    Child, Preschool
    Flow Cytometry
    Focal Adhesion Kinase 2
    Guanine Nucleotide Exchange Factors
    Humans
    Immunologic Memory
    Lymphocyte Activation
    Mice
    Mice, Inbred BALB C
    Mice, Inbred C57BL
    Mice, Knockout
    Myeloid Differentiation Factor 88
    Neutrophils
    Phosphorylation
    STAT3 Transcription Factor
    Toll-Like Receptor 9
    src-Family Kinases
    Immunology and Infectious Disease
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    Link to Full Text
    http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3362684/pdf/nihms370048.pdf
    Abstract
    The adaptors DOCK8 and MyD88 have been linked to serological memory. Here we report that DOCK8-deficient patients had impaired antibody responses and considerably fewer CD27(+) memory B cells. B cell proliferation and immunoglobulin production driven by Toll-like receptor 9 (TLR9) were considerably lower in DOCK8-deficient B cells, but those driven by the costimulatory molecule CD40 were not. In contrast, TLR9-driven expression of AICDA (which encodes the cytidine deaminase AID), the immunoglobulin receptor CD23 and the costimulatory molecule CD86 and activation of the transcription factor NF-kappaB, the kinase p38 and the GTPase Rac1 were intact. DOCK8 associated constitutively with MyD88 and the tyrosine kinase Pyk2 in normal B cells. After ligation of TLR9, DOCK8 became tyrosine-phosphorylated by Pyk2, bound the Src-family kinase Lyn and linked TLR9 to a Src-kinase Syk-transcription factor STAT3 cascade essential for TLR9-driven B cell proliferation and differentiation. Thus, DOCK8 functions as an adaptor in a TLR9-MyD88 signaling pathway in B cells.
    Source
    Nat Immunol. 2012 May 13;13(6):612-20. doi: 10.1038/ni.2305. Link to article on publisher's site
    DOI
    10.1038/ni.2305
    Permanent Link to this Item
    http://hdl.handle.net/20.500.14038/34921
    PubMed ID
    22581261
    Related Resources
    Link to Article in PubMed
    ae974a485f413a2113503eed53cd6c53
    10.1038/ni.2305
    Scopus Count
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