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Australian discovery on B Cells and Autoimmunity

Discussion in 'Other Health News and Research' started by Adster, Nov 8, 2012.

  1. alex3619

    alex3619 Senior Member

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    Logan, Queensland, Australia
    I think this shows that adjuvants can cause increased clonal expansion of B and T cells - in other words, we make more of them. In the case of autoimmunity this is not a cause, but might make it more severe.
     
  2. alex3619

    alex3619 Senior Member

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    Hi Lynne, I am trying to figure out which other thread. I do have over 3000 posts. If you have a specific question maybe I can answer it again. Bye, Alex
     
  3. natasa778

    natasa778 Senior Member

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    Thanks! Sorry I meant do these new findings by Garvan team link in to lymphoid hyperplasias and lymphomas we see?

    Re vaccines, would live attenuated ones carry a larger risk of autoimmune reactions in this scenario? (esp if immune system 'a bit' dysfunctional to start with?)
     
  4. alex3619

    alex3619 Senior Member

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    Hi natasa778, first about attenuated vaccines. This is only a guess, but I think the risk would indeed be higher. This is because there is an increased range of possible epitopes in an attentuated vaccine as opposed to one based on viral fragments.

    I do not think the Garvan findings directly link to hyperplasias and lymphomas. I think this is a different problem, even though it involves similar cells. I would need to know more about specific types of lymphomas than I do to say much more. What I can say is that some things trigger clonal expansion of B and T cells (and others) and I have two blogs planned for next year that relate to part of this, one on lipopolysacharide, and the other on gamma delta T cells. Gamma delta T cells are pro-healing cells that can increase or decrease the immune response in a region, depending on the nature of what the triggers are. I think they are probably severely disturbed in ME.

    Bye, Alex
     
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  5. Lynne B

    Lynne B Senior Member

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    Sorry, Alex, I was clearly in a state of severe confusion yesterday, very stressed about learning computer systems new to me. I thought your explanation on germinal centres was very clear. It actually appears in this thread.

    thanks, Lynne
     
  6. Hip

    Hip Senior Member

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  7. Hip

    Hip Senior Member

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    On reading the results of Chan, Brink et al, one thought that occurred to me is this:

    Lymph nodes are generally swollen in ME/CFS (lymphadenopathy is the technical term for swollen lymph nodes).

    Could lymph node swelling to some extent block the lymph node's access to the "outside world", ie, to the rest of the body, effectively making the germinal centers within the lymph nodes more distant from the target self-antigens of the autoantibodies?

    If so, the swollen lymph nodes of ME/CFS may be, in part, causing the autoimmunity and autoantibodies of ME/CFS.

    Thus some form of lymph node treatment that addresses the swelling (and the supposed blocked of state of the lymph node) may be helpful for ME/CFS.

    This also ties in with Raymond Perrin's view that lymphatic congestion and dysfunction is a causal factor in ME/CFS. The idea could be that lymphatic congestion blocks a lymph node's access to the rest of the body.

    And I wonder what would happen if you injected minute quantities of your body's own target self-antigens into your lymph nodes? Would that instantly switch off the autoimmunity and autoantibody production?



    Two known self-antigens in ME/CFS are cardiolipin antibodies 1 (cardiolipin is found on the inner mitochondrial membranes), and muscarinic receptor antibodies 1 (these muscarinic receptors are found on the postganglionic sections of the parasympathetic nervous system). In both cases, these self-antigens are ubiquitous, and found all over the body, so they would not be very physically distant from the germinal centers within the lymph nodes.
     

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