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Autoimmunity as a Consequence of Retrovirus-Mediated Expression of C-FLIP in Lymphocytes

Discussion in 'Other Health News and Research' started by Overstressed, Sep 20, 2012.

  1. Overstressed

    Overstressed Senior Member

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    Belgium
    I have no access to the full article, but the abstract is interesting to say the least. It describes the expression of a protein and the accumulation of activated B-cells.

    It's interesting in the context of what Dr. Ian Lipkin said in the press-conference, i.e., polyclonal activation of B-cells...

    Here's the abstract:
    http://www.cell.com/immunity/abstract/S1074-7613(00)80150-8


    Best regards,
    OS.
     
    heapsreal likes this.
  2. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    c-FLIP can also be initiated by LPS (lipopolysaccharide) and NFkB I think, though I would have to do some reading to be sure. Both LPS and NFkB appear to be elevated in ME. So this fits with known ME and CFS biochemistry. Bye, Alex
     
  3. lansbergen

    lansbergen Senior Member

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    http://www.ncbi.nlm.nih.gov/pubmed/21871974

    Autoimmune disease: A role for new anti-viral therapies?

    Dreyfus DH.
    Source

    Pediatrics, Yale University School of Medicine, New Haven, CT, United States. dhdreyfus@pol.net
    Abstract

    Many chronic human diseases may have an underlying autoimmune mechanism. In this review, the author presents a case of autoimmune CIU (chronic idiopathic urticaria) in stable remission after therapy with a retroviral integrase inhibitor, raltegravir (Isentress). Previous reports located using the search terms "autoimmunity" and "anti-viral" and related topics in the pubmed data-base are reviewed suggesting that novel anti-viral agents such as retroviral integrase inhibitors, gene silencing therapies and eventually vaccines may provide new options for anti-viral therapy of autoimmune diseases.
    Cited epidemiologic and experimental evidence suggests that increased replication of epigenomic viral pathogens such as Epstein-Barr Virus (EBV) in chronic human autoimmune diseases such as rheumatoid arthritis (RA), systemic lupus Erythematosus (SLE), and multiple sclerosis (MS) may activate endogenous human retroviruses (HERV) as a pathologic mechanism.
    Memory B cells are the reservoir of infection of EBV and also express endogenous retroviruses, thus depletion of memory b-lymphocytes by monoclonal antibodies (Rituximab) may have therapeutic anti-viral effects in addition to effects on B-lymphocyte presentation of both EBV and HERV superantigens. Other novel anti-viral therapies of chronic autoimmune diseases,
    such as retroviral integrase inhibitors, could be effective, although not without risk.
     

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