I talk to myself a lot.....I have 2 sons! I think some clarity is needed (for myself especially) so here goes. Below are 2 kit inserts for Immunology autimmune disease screenings which I picked up from the Immunology dep't at work. If you have had auto Ab screening some of your reactive tests might be here,the first scan is Autoimmune Inflammatory Myopathies 16Ag (IgG) The second insert is Antibodies against neuronal antigens (IgG) (Paraneoplastic syndromes 12 Ag) Why have I included these? Well, the obvious point is that there are no Ab here to a disease called myalgic encephalomyelitis! This won't shock the community to find out there is no diagnostic tool of this sort for ME/CFS. Therefore, I would hesitate to spend my £/$ on testing that cannot tell a biomed/doctor whether you have this disease, he/she could only tell you that you have Ab against anything in this panel- and that might not be of clinical significance anyway.....see later. There has been a study in Germany which targeted Beta 2 adrenergic Ab or B2AR (associated with POTS, Orthostatic hypotension) and M3 and M4 muscarinic cholinergic receptors. So it appears there may be auto Ab associated with ME. We need more if we are to develop an efficient method of diagnosis and monitoring. Is ME/CFS an autoimmune disease anyway? Is there a sub group of patients with autoimmune disease? Let's take a look at the sex distribution ratio in some autoimmune diseases. In SLE (Lupus) female to male ratio is approx 12:1 In MS (multiple sclerosis) it is 3:1 In RA (rheumatoid arthritis) it is 4.5 to 1 below age 50 In ME/CFS it is 3.5:1 So ME does fit the pattern of autoimmune disease in this respect though it is more than circumstantial it is not definitive proof even taking into consideration the German findings regarding B2AR. What is relevant however is that Rituximab is used (outside of cancer) primarily as a drug to target autoimmune disease so we might tentatively strengthen our hypothesis that ME is an autoimmune disease. This evidence is reinforced in the German study by the fact that lower levels of B2AR and M4 were found in ME patients following the course of rituximab treatment. Indeed, 60% of these patients were in full or partial remission 5 months following treatment. So can we build a hypothesis that ME/CFS is an autoimmune disease? Would new Ab discoveries lead us to be able to correlate areas of neuroinflammation that I outlined in the neurological forum diagrams with disruption of specific functional brain loci thus linking the Ab disruption with ME symptoms? Could we replicate the findings of the German team? The case is strong but I suspect we need the elucidation of many more auto Ab. to thymus etc Moving on to a read of a paper called Brain-reactive antibodies and disease by Diamond et al 2013 Annual review of Immunolgy, here are some pertinent points. Quoted or paraphrased The presence of CNS reactive Ab in general is harmless to the host Most brain reactive Ab appear to target antigens (Ag) expressed by neurons or astrocytes rather than Ag expressed by microglia. Microglia are the major phagocyte cell poulation of the CNS Ab in CSF may be a marker but not a contributor to pathogenesis therefore a patient may have elevated Ab but no disease. I've just tried to shed some light on our speculation. There is a great deal not known about brain function. There is evidence to suggest ME is an autoimmune disease of the brain. It is possible to argue against this hypothesis but worth pointing out that should the model of initial brain infection by EBV, CMV or gram -ve bacteria be responsible for stimulating a cascade that results in autoimmune disease then according to Diamond et al our prognosis may not be very positive- The brain has little regenerative capacity'. Is this why only such a small percentage of adult ME patients recover their health to pre ME levels and 90% of us don't? @Hip @Gingerggrl '