The above statement seems to suggest the reason some ME/CFS patients do not respond to rituximab is not because those non-responders have some non-autoimmune subtype of ME/CFS, but because for some reason, the rituximab did not work for these patients, and was not able to reduce the patients' production of autoantibodies.
In other words, even in the rituximab non-responders, their ME/CFS may still be autoimmune in nature.
That is not to say that the β2 and M4 autoantibodies are the cause of ME/CFS; ME/CFS may be caused by some other autoantibodies in the blood; but if rituximab is doing its job, it will reduce the level of all autoantibodies, so measuring the reduction in the β2 and M4 autoantibodies is just a gauge of whether rituximab is working.
@Jonathan Edwards, am I on the right lines here?
If the rituximab non-responders are indeed patients in which rituximab has failed to curb their autoimmunity, is there anything further that can be done in such cases? If these patients still have their ME/CFS caused by autoimmunity, can the autoimmunity be tackled in other ways if rituximab fails?
And do we know why rituximab fails to reduce levels of autoantibodies in some patients?