A hallmark of many autoimmune diseases, autoantibodies wreak havoc by recognizing and interfering with the body’s own proteins, DNA, and other molecules, known altogether as self-antigens.
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Evidence of a link between autoantibodies and long COVID symptoms is also building. Among the most incriminating are autoantibodies that bind to cell surface proteins called G-protein coupled receptors (GPCRs) and may block the messages these proteins convey to cells to control immune and other functions. Various GPCR antibodies are thought to contribute to ADs including ME/CFS, rheumatoid arthritis, and Sjogren’s syndrome. Last spring, a small study of individuals experiencing long COVID symptoms—particularly neurological (fatigue, etc) and cardiovascular (elevated heart rate, etc)—found that all had GPCR autoantibodies [9].
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If it can be demonstrated that certain autoantibodies are associated with specific symptoms of long COVID, “that would help strengthen the case” that there is an underlying autoimmune cause, Dr. Luning Prak says. In the context of acute COVID-19, there is evidence of autoantibodies targeting a range of self-antigens in the lungs, central nervous system, and other organs that have been implicated in long COVID disease.
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Last year, doctors gave a 59-year- old man an experimental drug for his glaucoma that blocks GPCR autoantibodies [17]. The patient also suffered from long COVID and had autoantibodies against GPCRs. In addition to improvements in his glaucoma, the man recovered from fatigue, brain fog, and loss of taste for at least 4 weeks.
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This quote is from the same website:"When you have an autoimmune disease, however, your immune system activates in an inappropriate or abnormal manner. Unable to distinguish between self and non-self proteins, a dysfunctional immune system mistakes the body’s own cells for harmful invaders. It produces cells and antibodies that target, attack, and damage healthy cells, tissues, and organs. "
Now I think that there is a fundamental error here - "It produces cells and antibodies that target, attack, and damage healthy cells, tissues, and organs. "
My understanding is, and please correct me if I am wrong, that antibodies do not target and attack and damage. I thought that antibodies came after the attack by the immune system and that their role is to clean up the debris left.
If my understanding is correct then I would have little belief in anything from The Global Autoimmune Institute if their basics are wrong:
i was just reading some of the reference papers quoted in this article . (because i was curious to see what evidence the suggestion that cfs is 'an autoimmune disease' was based on)
any way ... it's apparent that they are talking about an awful lot of different sorts of antibody (auto antibody ?) most of which i've not heard of before and don't know how they work at all .
it's extremely complex stuff , so we shouldn't assume that just because we understand that TPOab / TGab are 'markers' rather than 'attackers' , that all other antibodies work in same way .
eg it made me realise i'm not even very clear about the difference between an antibody , and an auto-antibody.
The references did lead me to some other interesting papers .. but i can't understand most of them because i don't know enough about 'immunity' to know what they mean..
after spending a little while this morning reading some of the links for this article , and then following some of the links those led too ...... it confirms why nobody has really figured out how the autoimmune part of our disease actually works yet , or it's cause or cure ..... the whole subject of immunity and autoimmunity is extremely flippin complicated .
i'm going to stick to something that is simpler eg . go and make some coffee then hang my washing out
As far as I have understood, an antibody is an antibody is an antibody. (Although there are five classes: IgA, IgD, IgG, IgE, IgM.
But when we are talking about blood tests, etc., I think we are taking about IgG soluble antibodies!
The issue regarding "auto" is whether its antigen (what it will recognise and stick to) is our own bodies, or something else. Such as a bacterium or virus or a molecule.
But this is somewhat complicated by the concept of "self"! A thyroid peroxidase antibody recognises a thyroid peroxidase molecule - but cannot know if that was produced by you - or not. (Just illustration - other than from a blood transfusion, no-one would inject IgG.)
also .. just realised it say's " produces cells AND antibodies that target ,attack ,and damage" ..... they don't specify in this sentence if 'the cells' or 'the antibodies' are responsible for any particular action.. eg 'target ' could be interpreted quite broadly
I'm just exasperated that LC is eliciting all this research, whilst people suffering from ongoing fatigue conditions have very little care or investigation beyond placating therapies like cognitive behavioural therapy🙄 and highly contentious and somewhat diabolical 'graded exercise therapy'. Up until now, the most the majority of such people ever received was a patronising dismissal by their GP and a prescription for anti- depressants. That is what they are giving anyone with fibromyalgia, post viral exhaustion or chronic fatigue. Mostly grandfather ADs, and if you're also in pain and you beg for it consistently, possibly tramadol, gaberpentin, etc.
It's grossly unfair. But I hope they widen the scope of application of any useful findings to other groups besides that of LC and GPs keep abreast of the latest research.
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