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Trigger identified that likely unleashes autoimmune disease

Discussion in 'Other Health News and Research' started by deleder2k, May 16, 2015.

  1. deleder2k

    deleder2k Senior Member

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    Australian researchers believe they have discovered a group of cells that trigger autoimmune disease, as well as the molecular 'trigger guard' that normally holds them in check.

    Source: ScienceDaily.com

    Published in the respected journal "Immunity" (impact factor 19.748 as of 2013)

    @Jonathan Edwards, what do you think of the research conducted Down Under? Are they into something, and is it plausible that rogue germinal centre B cells could pave the way for ME?
     
    Last edited: May 16, 2015
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  2. Marco

    Marco Grrrrrrr!

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    Does this then suggest a genetic/epigenetic element to some autoimmune diseases even though the production of rogue germinal B cells is random?
     
  3. snowathlete

    snowathlete

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    Very interesting, especially the IgE link.
     
  4. Snow Leopard

    Snow Leopard Hibernating

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    Yes, of course.

    The model that these researchers developed however, generated a lot of IgE antibodies rather than IgG, and so this particular finding may only be relevant to autoimmune conditions where IgE antibodies are implicated in the disease.
     
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  5. msf

    msf Senior Member

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    It seems to be an explanation for some autoimmune diseases rather than all autoimmune diseases. From what I've just read, ALPS is usually diagnosed early in life, which would seem to make FAS mutations a unlikely cause of autoimmune diseases that develop later in life.
     
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  6. Jonathan Edwards

    Jonathan Edwards Senior Member

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    A bit odd really. My own group suggested that autoimmunity was due to rogue germinal centre B cells in 1999 so that does not seem very new! And Fas defects causing autoimmunity in mice with lymphoproliferation has been around since the lpr gene was found in MRL/lpr mice around 1982. Maybe this group have not realised they have re-invented a well known spontaneous mutant model.

    As Snow Leopard points out, the difficulty in relating this to human autoimmunity is the focus on IgE. IgE is not really a feature of human autoimmunity. You can find IgE autoantibodies if you look hard but none of the autoimmune disease I know of use IgE effector mechanisms. And at a simpler level, humans with autoimmunity do not have Fas defects. I think we told a rather better story in 1999 that makes a bit more sense than this. What immunological colleagues never seemed to 'get' is that the rogue cells in autoimmunity are completely normal in all respects except the antibody they make. Colleagues would hold up there hands in horror and say 'why should their be rogue mutating cells in autoimmunity - what would cause it?'. The simple answer is that mutating is what B cells do for a living so you do not need any special cause or trigger. You just need the antibody to crash the regulatory system.

    So the title of this piece is certainly wrong I think - this is not the trigger for human autoimmune disease - because humans don't have the Fas defect and there ain't no trigger.
     
  7. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Another point is that Fas defect animals get every autoimmune problem under the sun. Humans get one at a time - or occasionally a couple of associated ones.
     
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  8. Marco

    Marco Grrrrrrr!

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    So basically this is a FAS defect disease that affects apoptosis of cells which may include rogue B cells rather than an autoimmune disease per se?

    Maybe I've got the wrong end of the stick.
     
  9. Jonathan Edwards

    Jonathan Edwards Senior Member

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    Seems more towards the right end to me. It becomes semantic, but these poor animals have a lot more problems than just autoantibodies.
     
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