@Jonathan Edwards do you think that cluster outbreaks are a different disease / subgroup to individual isolated cases ?
My Rituximab experience for ME
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I think we are running into problems with confusing arguments about autoimmunity with arguments about ME. If there are half a dozen ways to get the clinical pattern of "CFS' (maybe through 6 different 'MEs') some of which are autoimmune and some not then we can't expect arguments about autoimmunity to hold for all ME. Moreover, it is quite possible that one of many autoimmune diseases - maybe ME - IS triggered by virus when all the others are not. The previous posts were about autoimmunity and EBV in general if I remember rightly. My experience with trying to tease out the causal mechanisms of these diseases is that you have to make sure you do not wander from one argument to another or one disease to another without noticing.
Indeed, but how do we know what disease we are talking about when we can't identify it ?
Should we give them names ... Autoimmune ME, cluster ME, EBV ME, immune dysregulation ME, etc. ? Without such or some definition I think you are right, many discussions will wander off because not every disease type will fit the discussion and everyone wants to apply their type or idea or theory to the discussion.....
Just one of the many inconveniences of this disease!
Should we give them names ... Autoimmune ME, cluster ME, EBV ME, immune dysregulation ME, etc. ? Without such or some definition I think you are right, many discussions will wander off because not every disease type will fit the discussion and everyone wants to apply their type or idea or theory to the discussion.....
Just one of the many inconveniences of this disease!
My opinion is I don't think we can be either surprised or unsurprised when it comes to disease or indeed nature.... It is what it is and if randomness plays a part then why would I be surprised at anything.... Anything is possible and once you believe that then the surprise is gone ... Just my way of looking at things.
It's only lucky if you and they are right 
In general all research is good because it might indicate a biomarker or it might disprove a theory ... Either result is positive if it helps get us to and end result. It doesn't matter too much who is right or wrong on this forum, but we are all entitled to our opinions and different opinions may be right.
In general all research is good because it might indicate a biomarker or it might disprove a theory ... Either result is positive if it helps get us to and end result. It doesn't matter too much who is right or wrong on this forum, but we are all entitled to our opinions and different opinions may be right.
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We were talking about well known diseases I think - RA or lupus or whatever. Then the discussion got mixed up with ME. I have given my guess of the different MEs we might be trying to pin down, in the thread on MEs causing CFS. I certainly wouldn't want to start with assumption that there is 'a disease' called ME, just a syndrome of CFS that is likely to have several routes in. At the moment we are having to relate evidence to the syndrome of CFS in effect. But maybe we are on the margin of being able to be a bit more precise in terms of autoimmune routes. I also tend to think that there is a CFS subset that goes with the T cell related spondarthropathy cluster, which is not autoimmune.
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I don't think we have reason to think we can create any of these diseases in a lab to be honest. The main message I take from the presence of 100 different animal models of RA is that since 99 of them must be on the wrong tack it is pretty likely that 100 are.
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Are there infectious diseases in lab animals that generate autoimmunity? There may be but I am not sure I can think of any. You can certainly get adverse immune responses to things like streptococci, with post-infective complications, but I don't see that as relevant to autoimmunity of the human sort, with long term autoantibody production mediating disease.
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Spondarthropathy includes reactive arthritis and is not associated with autoantibodies or autoimmunity as far as we know. It can be triggered by infection.
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I agree that this is interesting but I am not convinced this is infection causing autoimmune disease. A number of chronic infections cause polyclonal B cell activation which often includes production of rheumatoid factor, for instance. Rheumatoid factor is an autoantibody, but in these chronic infectious states (bacterial endocarditis, Hepatitis C) it does not appear to cause any disease. It is a sort of epidphenomenon. Chagas disease produces polyclonal B cell activation. The autoantibodies recently discussed seem to turn up in a lot of clinical contexts and may, like rheumatoid factor or ANA, be 'easily produced' (or even, in the case of RF 'physiological') autoantibodies that are not necessarily of any pathogenic importance.
I always find your answers very interesting, Prof, Edwards, but they always make me want to ask more questions...how can autoantibodies cause disease in some cases but not in others? You said in the other thread that there isn´t a strong correlation with the level of antibodies, so is it a binding thing?