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killing T-regs causes more immune suppression than letting them live.

Discussion in 'Other Health News and Research' started by anciendaze, Oct 30, 2017.

  1. anciendaze

    anciendaze Senior Member

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    By now you've heard many strange stories about odd behavior of different classes of immune cells, if you've been interested in following research on them, as I am. Here's a discovery made at University of Michigan about cancer therapy which reveals why previous theories of immune activity which showed that T-reg cells were limiting immunotherapy against cancer cells failed to improve matters.

    If T-regs are preventing therapy, we'll just kill them off, right? Instead, things got worse, because dying T-regs signaled to cause even more inhibition of immune activity.

    Why am I posting this here? The signals came from dying cells releasing ATP, purinergic signalling. What else does ATP do? Well, it is sort of important in energy production (metabolism).

    We have another link here between dysfunctional immune regulation and metabolomics.
     
    pibee, bspg, Murph and 10 others like this.
  2. Jesse2233

    Jesse2233 Senior Member

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    Interesting... I wonder if this would contraindicate photopheresis
     
  3. melihtas

    melihtas Senior Member

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    I think this explains why ME patients got worse for a few months before getting better in Cyclophosphamide trial.
     
    Murph, ErdemX and ukxmrv like this.
  4. Murph

    Murph :)

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    This is bad news for a promising cancer treatment but good news for me/cfs, really. The fact the immune system is now so central to oncology and immunology dramatically increases the chances that a serendipitous finding from a well-funded and well-staffed field will light up the pathways implicated in me/cfs and make a whole lot of things fall into place.

    here's an excerpt from the article linked above:

    >"It's a double-edged sword: If they do not die, they are suppressive. But if they die, they are even more suppressive," says senior study author Weiping Zou, M.D., Ph.D., Charles B. de Nancrede Professor of surgery, immunology, pathology and cancer biology at the University of Michigan.

    >"Nobody expected this - it was a total surprise. But it likely explains why you don't see benefit when you induce Treg apoptosis," he says.

    >Immunotherapy has revolutionized cancer treatment, but limitations and questions remain. One of the biggest questions is why such a small number of patients are responsive.

    >In 2004, Zou's lab discovered that Treg cells were acting against cancer immunity. They linked higher numbers of these cells to shorter survival in patients. That work led to the failed clinical trial designed to eliminate the Treg cells.

    >It turns out, this new study finds, that when Treg cells die, they release a lot of small metabolites called ATP. Usually ATP helps supply the body with energy. But dying Tregs quickly convert ATP to adenosine. The adenosine then targets T-cells, binding to a receptor on the T-cell surface. This affects the function of the T-cells, making them unhealthy."
     
  5. bspg

    bspg Plant Queen

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    Thank you for posting this @anciendaze. I read this article yesterday and was thinking the same thing about purigenic signaling. I wonder if these dying tregs could be implicated in ME/CFS.
     
    Learner1 likes this.
  6. anciendaze

    anciendaze Senior Member

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    There is a great deal more to be learned about purinergic signalling, and this is important for a variety of reasons connected with the fundamental role of purines in cell metabolism. Often such releases act as a confirmation signal indicating that something happening somewhere in the body is affecting cells nearby, and thus of interest to a particular cell. This is a problem for tests that assume peripheral blood drawn from a distant place gives the whole story about what is going on at some other place.

    What it looks like to me is that this unexpected response plays a significant role in limiting autoimmunity. We tend to forget that cancer cells have virtually all the characteristics of "self", not other. This mechanism might also be important in autoimmune diseases, where medical progress has been disappointing in terms of new treatment options. With this finding at the crossroads of oncology and rheumatology it should receive increased funding, assuming scientific research doesn't simply go out of business.
     

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