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    block this user Werner Muller

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    Faculty of Life Science, University of Manchester, Manchester

    LMP1 signaling can replace CD40 signaling in B cells in vivo and has unique features of inducing class-switch recombination to IgG1.

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    The Epstein-Barr virus (EBV) protein LMP1 is considered to be a functional homologue of the CD40 receptor. However, in contrast to the latter, LMP1 is a constitutively active signaling molecule. To compare B cell-specific LMP1 and CD40 signaling in an unambiguous manner, we generated transgenic mice conditionally expressing a CD40/LMP1 fusion protein, which retained the LMP1 cytoplasmic tail but has lost the constitutive activity of LMP1 and needs to be activated by the CD40 ligand. We show that LMP1 signaling can completely substitute CD40 signaling in B cells, leading to normal B-cell development, activation, and immune responses including class-switch recombination, germinal center formation, and somatic hypermutation. In addition, the LMP1-signaling domain has a unique property in that it can induce class-switch recombination to IgG1 independent of cytokines. Thus, our data indicate that LMP1 has evolved to imitate T-helper cell function allowing activation, proliferation, and differentiation of EBV-infected B cells independent of T cells.

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    Description

    Title : LMP1 signaling can replace CD40 signaling in B cells in vivo and has unique features of inducing class-switch recombination to IgG1.
    Author(s) : Julia Rastelli, Cornelia Hömig-Hölzel, Jane Seagal, Werner Müller, Andrea C Hermann, Klaus Rajewsky, Ursula Zimber-Strobl
    Abstract : The Epstein-Barr virus (EBV) protein LMP1 is considered to be a functional homologue of the CD40 receptor. However, in contrast to the latter, LMP1 is a constitutively active signaling molecule. To compare B cell-specific LMP1 and CD40 signaling in an unambiguous manner, we generated transgenic mice conditionally expressing a CD40/LMP1 fusion protein, which retained the LMP1 cytoplasmic tail but has lost the constitutive activity of LMP1 and needs to be activated by the CD40 ligand. We show that LMP1 signaling can completely substitute CD40 signaling in B cells, leading to normal B-cell development, activation, and immune responses including class-switch recombination, germinal center formation, and somatic hypermutation. In addition, the LMP1-signaling domain has a unique property in that it can induce class-switch recombination to IgG1 independent of cytokines. Thus, our data indicate that LMP1 has evolved to imitate T-helper cell function allowing activation, proliferation, and differentiation of EBV-infected B cells independent of T cells.
    Keywords : animals, antibodies, antibodies immunology, antigens, cd40, cd40 deficiency, cd40 genetics, cd40 immunology, cd40 metabolism, b lymphocytes, b lymphocytes immunology, cells, cultured, enzyme activation, germinal center, germinal center immunology, germina

    Subject : unspecified
    Area : Other
    Language : English
    Year : 2008

    Affiliations Faculty of Life Science, University of Manchester, Manchester
    Journal : Blood
    Volume : 111
    Issue : 3
    Pages : 1448-1455
    Url : http://www.ncbi.nlm.nih.gov/pubmed/18006702

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    Werner's Peer Evaluation activity

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