So the question ist whether it is the immune system causing ME or the over- or underactivity of the immune system is only a consequence of ME. Personally, because of the two (or perhaps: three) groups of ME-sufferers, it might be the latter. Or if ME is an autoimmune disease itself (but if that is the case, shouldn't there be any inflammation?)
Auto immunity and an underactive immune system is quite common. I know that from other psoriasis sufferers. But what I find interesting is whether the auto immunity group would have better response to rituximab than the other group. Is there any discussion about that? And: I have read from some doctors that they find there is always a chronic infection going on in ME patients.
First, I suspect many of us harbor infections of some sort, whether or not our doctors have found them. Many doctors don't bother to look, and others are mistaken in their interpretation of the labs and tell patients they don't have an infection when its there.
And most of these infections are no longer acute, but rather the chronic, smoldering kind that destroy our health by hijacking resources, damaging tissues, mingling with our DNA and RNA, and in many cases, triggering autoimmune antibodies.
Mark Davis, at the OMF Symposium, gave s brief layperson's overview of the antibody toolkit we're born with, so that we can create antibodies from building blocks to anything we encounter. Sometimes, the body inappropriately makes antibodies to thins it shouldn't, as in Hashimotos, lupus, etc.
And some of us are more genetically prone to making antibodies. In going through my health history, my ME/CFS specialist noted I had Hashimotos, celiac, and multiple food allergies and immediately created an action item to see if I had antibodies that have been noted in ME/CFS patients, which I did.
Depending on the status of these infections and autoimmune antibodies, our level of inflammation may vary, from very little to quite a lot and it may vary through our the body, with more in the brain, more in the gut, or less in other places, for example.
Therefore, there's no one-size-fits-all solution, its a matter of treating us as individuals.
As for Rituximab, I'm still learning, but it seems that one needs to clear any infections as much as possible first, then use Rituximab to wipe out the B cells with the troublesome antibodies. That's why a few doctors are starting people with IVIG and antivirals/antibiotics/LDN, then moving to Rituximab.
None of this is commonplace, its very experimental, and there are significant side effects and risks involved.
It is worth getting the best diagnosis you can and thoroughly researching all possible treatment modalities as there are situations where the risks can be fatal or at least very damaging. (My current opinion...)
That's why looking at 10-pass ozone might be a possibility. And then there are various stem cell transplants, which are quite controversial. And a long list of other treatments that may work for some if us, yet not for others.