How long before the body clears autoantibodies itself? (And my Cell Trend results)

[crussher]

Hi everyone,

I got the Cell Trend labs done for POTS & ME autoantibodies. I came back positive for all the autoantibodies associated with ME/CFS. These were those results:

Anti B 1 adrenergic receptor autoantibodies 17.4 (Positive = >15)
Anti B2 adrenergic receptor autoantibodies 22.3 (Positive = >14)

Anti muscarinic cholinergic receptor autoantibodies 3 11.4 (Positive = 10)
Anti muscarinic cholinergic receptor autoantibodies 4 15.9 (Positive = 10.7)

I'm looking into what all these mean now. I know from Scheibenbogen's research that the AntiB2 aabs prevent normal vasodilation and thereby blood perfusion. I've also just learnt that anti-muscarinic means 'anti parasympathetic' and that these aabs prevent rest and digest functions of the ANS.

Anyway, I wanted to know if there is anyone here who might be able to answer the following question:

If you managed to stop the source of these autoantibodies, i.e. what is creating them in the first place, how long would it then take the body to clear the autoantibodies that are already there? IE: what is the natural life-cycle time of an autoantibody and how long does it take for the body to clear it?

Thanks to anyone who can help.

 

[Osaca]

I remember reading somewhere, that they have a lifetime of roughly 10-20 days. So the problem isn't their existence, but rather their production by B-cells. I don't have a source for this lifetime right now.

In general you won't manage to stop the source of the autoantibodies that is the whole problem, unless you do something like B-cell depletion, for which there is no guarantee of working. If we could stop the source than we would just be doing that instead of Immunadsorption(+B-cell depletion) or waiting for BC007.

Scheibenbogen is planning to do Immunadsorption+B-cell depletion if her Immunadsorption trial shows positive results.

 

[crussher]

I remember reading somewhere, that they have a lifetime of roughly 10-20 days. So the problem isn't their existence, but rather their production by B-cells. I don't have a source for this lifetime right now.

In general you won't manage to stop the source of the autoantibodies that is the whole problem, unless you do something like B-cell depletion, for which there is no guarantee of working. If we could stop the source than we would just be doing that instead of Immunadsorption(+B-cell depletion) or waiting for BC007.

Scheibenbogen is planning to do Immunadsorption+B-cell depletion if her Immunadsorption trial shows positive results.

Thank you very much for this - that’s really helped me understand things better.

Is there a link between the particular antibodies B cells produce and the autonomic nervous system? I can’t help but notice that the autoantibodies (that I was positive to) all seem to relate to sympathetic overdrive. I’m wondering if the dysautonomia that is part of ME/CFS might be leading the B cells to increase these specific autoantibodies.

 

[Osaca]

Thank you very much for this - that’s really helped me understand things better.

Is there a link between the particular antibodies B cells produce and the autonomic nervous system? I can’t help but notice that the autoantibodies (that I was positive to) all seem to relate to sympathetic overdrive. I’m wondering if the dysautonomia that is part of ME/CFS might be leading the B cells to increase these specific autoantibodies.

This post has all the relevant articles in connection to GPCR-AAB's and LC/ME/CFS www.reddit.com/r/covidlonghaulers/comments/120ko6n/bc007_and_gpcraabs_everything_we_dont_know.

A priori I have to warn you that your test results won't give you anything, especially since you did an ELISA test instead of an functional assay, which many believe to be superior. There is nothing you can currently do about your test results. You can't even say that they're positive because you're sick, since healthy people have them as well. Their functionalty is far more nuanced than higher levels and the environment in which they act seems crucial. For POTS (and not ME/CFS) there was even a study that showed that the levels of the CellTrend test were irrelevant.

Regarding GPCR-AAB's it is unfortunately the case that far more is unknown than known and it seems that they play a role in a subset of patients. They are central to the Scheibenbogen-Wurth hypothesis.

 

[linusbert]

Hi everyone,

I got the Cell Trend labs done for POTS & ME autoantibodies. I came back positive for all the autoantibodies associated with ME/CFS. These were those results:

Anti B 1 adrenergic receptor autoantibodies 17.4 (Positive = >15)
Anti B2 adrenergic receptor autoantibodies 22.3 (Positive = >14)

Anti muscarinic cholinergic receptor autoantibodies 3 11.4 (Positive = 10)
Anti muscarinic cholinergic receptor autoantibodies 4 15.9 (Positive = 10.7)

I'm looking into what all these mean now. I know from Scheibenbogen's research that the AntiB2 aabs prevent normal vasodilation and thereby blood perfusion. I've also just learnt that anti-muscarinic means 'anti parasympathetic' and that these aabs prevent rest and digest functions of the ANS.

Anyway, I wanted to know if there is anyone here who might be able to answer the following question:

If you managed to stop the source of these autoantibodies, i.e. what is creating them in the first place, how long would it then take the body to clear the autoantibodies that are already there? IE: what is the natural life-cycle time of an autoantibody and how long does it take for the body to clear it?

Thanks to anyone who can help.

i've read somewhere that retinol might be involved in immune system forgetting things again. but i do not remember any specifics. check the forum maybe you find it.

 

[gregh286]

Hi everyone,

I got the Cell Trend labs done for POTS & ME autoantibodies. I came back positive for all the autoantibodies associated with ME/CFS. These were those results:

Anti B 1 adrenergic receptor autoantibodies 17.4 (Positive = >15)
Anti B2 adrenergic receptor autoantibodies 22.3 (Positive = >14)

Anti muscarinic cholinergic receptor autoantibodies 3 11.4 (Positive = 10)
Anti muscarinic cholinergic receptor autoantibodies 4 15.9 (Positive = 10.7)

I'm looking into what all these mean now. I know from Scheibenbogen's research that the AntiB2 aabs prevent normal vasodilation and thereby blood perfusion. I've also just learnt that anti-muscarinic means 'anti parasympathetic' and that these aabs prevent rest and digest functions of the ANS.

Anyway, I wanted to know if there is anyone here who might be able to answer the following question:

If you managed to stop the source of these autoantibodies, i.e. what is creating them in the first place, how long would it then take the body to clear the autoantibodies that are already there? IE: what is the natural life-cycle time of an autoantibody and how long does it take for the body to clear it?

Thanks to anyone who can help.

Good.test that
Who or how collected your sample?
Around 3 weeks does seem to be the general consensus for 1/2 life on googling I did just now.

 

[JES]

Is there a link between the particular antibodies B cells produce and the autonomic nervous system? I can’t help but notice that the autoantibodies (that I was positive to) all seem to relate to sympathetic overdrive. I’m wondering if the dysautonomia that is part of ME/CFS might be leading the B cells to increase these specific autoantibodies.

Yes, there seems to be a connection, but it hasn't been established for sure unlike with certain other autoimmune diseases like myasthenia gravis, where autoantibodies targeting acetylcholine receptors have been established to be the cause.

With POTS and ANS dysfunction patients it seems a little more complicated as some test positive for a lot of the Cell Trend panel autoantibodies, while others don't. I personally tested high on every single one, which makes me fairly confident it's causing my issues.

The level of antibodies also seem to matter. I reckon my doctor specified that it was one of the anti-muscarinic ones, I reckon 4, which they had found some correlation for with symptoms when that value was over 50.

Regarding your final question. It could be, but I think it's more likely that those autoantibodies are actually the ones that whack the autonomic nervous system and not the other way around. Then there is of course a cause for those autoantibodies, which is the million dollar question. My guess is that the immune system is just dysfunctional due to either chronic infection or some kind of autoimmunity, for example due to molecular mimicry.

 

[Osaca]

I just recalled that there was recently an international GPCR-AAB conference Scheibenbogen, Hohberger and the other specialists all participated. You might want to read throught the report. It is a good summary of what we know, but even more so about how little we know about GPCR-AAB's https://www.sciencedirect.com/science/article/abs/pii/S1568997223000447.

 

[crussher]

A priori I have to warn you that your test results won't give you anything, especially since you did an ELISA test instead of an functional assay, which many believe to be superior. There is nothing you can currently do about your test results. You can't even say that they're positive because you're sick, since healthy people have them as well. Their functionalty is far more nuanced than higher levels and the environment in which they act seems crucial. For POTS (and not ME/CFS) there was even a study that showed that the levels of the CellTrend test were irrelevant.

Thanks for these thoughts. I have looked at that study that compared AABS in POTS patients and in healthy controls. While the AABS were similar in both of those groups, the number of AABS in both groups in that study, eg with Beta2 AABS, appeared to still be much lower than my results, four times lower in fact. I think Scheibenbogen has also done a study which shows that AABS levels correlates with symptom severity though there was another study that perhaps suggested otherwise. I appreciate your points though - there is much that is not known.

 

[crussher]

Good.test that
Who or how collected your sample?
Around 3 weeks does seem to be the general consensus for 1/2 life on googling I did just now.

Thanks for the googling, great to know that. I am being treated for HELP apheresis in Bayreuth, Germany, and the nurse collected my sample at the start of a session and sent it to the Cell Trend lab in Luckenwalde. 10 days for the results.

 

[Osaca]

Thanks for the googling, great to know that. I am being treated for HELP apheresis in Bayreuth, Germany, and the nurse collected my sample at the start of a session and sent it to the Cell Trend lag in Luckenwalde. 10 days for the results.

Cool, is that at Beathe Jaeger's new lab?

 

[crussher]

Cool, is that at Beathe Jaeger's new lab?

I think Jaeger's new clinic will be in Bad Aibling. Bayreuth is a standard dialysis centre and HELP apheresis is a new treatment here since January with the arrival of Dr. Satanovskij, who previously oversaw HELP at a different clinic (Lorrach, I think)