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I can see how it could be one cause for autoimmunity but I don't think it's the only cause.
What do you make of this alleged evidence for molecular mimicry @Jonathan Edwards?
I think you'll find your answer here.
Yup. This presentation is a load of nonsense. The guy starts with a few anecdotes and then babbles on about how many bacteria we have in our guts for about half an hour. There is no content here. The Congress on Autoimmunity is pretty much a joke institution set up by phoneys years back - still running.
I did not listen to the whole thing but if there is actually any coherent argument in there do let me know! There is no mechanism by which infection can cause autoimmunity by mimicry that I am aware of. If a bacterium can cause an immune response by mimicry then presumably the host itself can cause a response by being identical to itself, even more easily. It makes no sense.
I think the only argument was that since those proteins looked identical on the "supermicroscope", then -> molecular mimicry exists.
Your last point was great, kind of a nail in the coffin as far as the logic of molecular mimicry is concerned..
I'm kind of on the fence about molecular mimicry, probably because I haven't spend a lot of time researching it, but I have to wonder, take mast cell serine proteases and fungal/mold serine proteases, say you in a water damaged building getting very ill and you immune system is trying hard to keep up and it's mass confusion going on in your body because theres a lot your getting exposed to all at one time, do you think the immune system can get confused?
what do you think about this?
Guillain-Barré Syndrome Animal Model: The First Proof of Molecular Mimicry in Human Autoimmune Disorder
http://www.ncbi.nlm.nih.gov/pubmed/21197269
http://www.hindawi.com/journals/bmri/2011/829129/
This is quoting work from Hugh Willison from nearly 20 years ago. Guillain Barre remains the one disease where it looks as if there might be a cross reaction with a pathogen. But note that the animal model is non sequitur - it proves nothing about what happens in the human. And whether there are really pathogenic autoantibodies in GB remains uncertain. And of course GB is very unlike autoimmune diseases where autoantibodies are well documented - it is a short lived monophasic process, even if recovery may be very slow and incomplete. If anything it seems to be the exception that probes the rule. I personally suspect it is more like rheumatic fever, where an antibody response to a pathogenic appears to throw up immune complexes with peculiar properties leading to joint and heart lesions. The idea that the immune response cross reacts with heart has never been substantiated and is almost certainly wrong.
well, I try to stay open minded to it but I just don't know, it does seem that it would be proven or further advanced by now, but setting here with ME/CFS and knowing theres so much unknown still, ?
[/QUOTE
Insights from the predicted epitope similarity between Mycobacterium tuberculosis virulent factors and its human homologs
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4702028/
Further there was a high structural similarity of M.tb SOD and human MnSOD at both primary and tertiary structure level
So, the molecular mimicry idea is rubbish, but possibly true in the case of Gullain-Barre Syndrome (which can also be a chronic condition)?
My head hurts. I think I need to go lie down.
Dear @osisposis,
What you have to remember is that people are mostly like sheep. They have no new ideas so they just follow everyone else - they vote for Donald Trump or Mr Osborne's austerity despite both being close to suicide.
Immunologists are people and by and large they cannot think of any new ideas - or even work out which of the old ideas make sense - so they keep writing about an idea that is fifty years old and never made sense or was supported by any evidence.
This paper is drivel. The journal is of the sort that will publish anything anyone wants to pay for publishing (these days you pay journals to publish your stuff so they are happy to print nonsense and rake in the money.) There is actuually no experiment here. Moreover, the abstract is full of nonsense statements. Rheumatoid arthritis and lupus have nothing to do with mycobacteria. There might be debate about prevotella copra but at a rheumatology meeting of 3,000 scientists you are unlikely to find anyone who thinks it has anything to do with mycobacteria. The authors are just making things up as they go along.
What the paper shows is that if you walk on a beach and pick up a pebble, after five years of walking you are pretty sure to find another pebble that looks just the same. Or that if a child were to come up saying look I found two pebbles exactly the same you would conclude that God knew about the first pebble and made the second one to match. Put another way, if you drive two thousand miles you are bound to find two car number plates that are exactly the same apart from one number or letter.
What I think is hard for people to understand, and this is part of the reason why I post here, is just how bad most scientific papers are these days. This is the equivalent of some high school kids trying to work out whether there is a Higgs boson - without knowing any physics.
And what is so sad is that MOST immunologists, although they can see this is rubbish, cannot see why the molecular mimicry idea is rubbish, despite the fact that it is barn door obvious - and at least Marky90 gets it!
Our bodies are full of proteins. All the time these proteins are being slightly damaged and eventually cleared away once they are too damaged. Amino acids get oxidised or cross linked or glycated. And every self protein that has been slightly changed is now 'almost identical to self' and so if molecular mimicry worked our immune system would constantly be mounting immune responses to these damaged proteins that cross reacted with good proteins and gave us total autoimmunity every day of the week. It simply cannot make sense. And since there is essentially no evidence for an association between infection and autoimmune disease that would fit with mimicry nobody should be surprised.
well , I hate Thrump with a passion, lols, and my research is totally my own, I don't follow anyone, and I understand what your saying about proteins, but also not everything is always that cut and dry, shit happens , I just keep a opened mind because you have to. and believe me, I know how bad some papers can be, I've spent many years wading though the muck, it drives me crazy that so many things are looked at ass backwards, you can not be a researcher without keeping a open mind. and everyday life exposures and being in a bad high moisture water damaged building exposure are not the same thing, very hard on the body, brain and immune system.
´Demonstrating that patients had nerve damage because of antibodies against bacteria cross reacting with nerves is a much harder task.´
Surely this, if proven, would qualify as autoimmunity, wouldn´t it?
This is the chronic condition I was referring to: http://www.ninds.nih.gov/disorders/cidp/cidp.htm
´The only real proof we have that autoantibodies cause disease comes from neonatal lupus, myasthenia and Ro syndrome (congenital heart block) where the antibodies come from the mother.´
Now I´m really confused. If autoantibodies don´t cause disease, what makes patients with autoimmune diseases ill?