De Meirleir is using Rituximab?

[Jonathan Edwards]

So how come an ongoing autoimmune disease ´needs´ an ongoing ´supply´ of antibodies, but an ongoing response to an ongoing infection (which is what I was suggesting) doesn´t?

Both require an ongoing supply of antibody if they are mediated by antibody. But antibody to foreign proteins does not cause unwanted effects in a chronic situation. Antibody - antigen complexes involving microbial proteins can cause renal damage in an acute reaction - as in serum sickness - but in the longer term it is extremely rare for foreign protein to be persistently available at relevant levels.

Thanks for the sepsis example. I guess some people thought it was worth a try though, which leads me to the next question: if dampening the response can help (as in your TB example), how can we be sure it won´t in any particular disease? It may be unlikely, but it still seems like a possibility worth keeping in mind.

It is theoretically possible but the empirical evidence we have from a wide range of diseases makes it very unlikely that it would be relevant to ME. None of the symptoms of ME look like antibody interactions with foreign proteins - which are stereotyped. The more interesting question is whether they might be due to antibody interactions with self proteins, which are not stereotyped because the symptom is different for each differentt self protein being interfered with.

 

[Emily L]

Thank you @Jonathan Edwards for this analysis

 

[msf]

Both require an ongoing supply of antibody if they are mediated by antibody. But antibody to foreign proteins does not cause unwanted effects in a chronic situation. Antibody - antigen complexes involving microbial proteins can cause renal damage in an acute reaction - as in serum sickness - but in the longer term it is extremely rare for foreign protein to be persistently available at relevant levels.



It is theoretically possible but the empirical evidence we have from a wide range of diseases makes it very unlikely that it would be relevant to ME. None of the symptoms of ME look like antibody interactions with foreign proteins - which are stereotyped. The more interesting question is whether they might be due to antibody interactions with self proteins, which are not stereotyped because the symptom is different for each differentt self protein being interfered with.

I thought it might be something to do with the availability of antigen, but what if the antigen was from a commensal organism? I am thinking along the lines of antibodies to various gram-negative commensal bacteria, as found by Maes. Also, does removing an antibody once an immune response has already been developed have an effect on other parts of the immune response, e.g. cytokine production? If not, I guess you may be right in saying there aren´t any signs of foreign antigen-antibody interaction in ME, but if it does, the flu-like symptoms would seem to suggest such a reaction, unless the flu-like symptoms people get when they have flu all derive from the other parts of the immune response.