It's my understanding that "immunosuppression" is pretty broad. There are many different cytokines, antibodies, etc, involved in immune activation and autoimmunity.
It's my understanding that cyclophosphamide confers quite broad immunosuppression. Sure there are selective drugs like rituximab, but in general the DMARDs and 5-ASA drugs all act fairly broadly. There are the TNF inhibitors and newer gen biologics, but generally we don't have a ton of tools off the shelf for selective immunosuppression.
The first step in curing the disease will be to identify the specific parts of the immune system that are dysregulated and why this is the case. But until then people need treatment ASAP and if cycloME is any indication (as well as anecdotes about corticosteroids), then maybe the less severe patients will benefit from drugs like azathioprine, sulfasalazine, and plaquenil. Isn't Klimas doing a trial involving a TNF inhibitor at this time?
Some people with ME/CFS have both low total IgG and high IgG bands...
I'm just speculating here but as the immune system is a multivariate nonlinear system, it's possible the abnormal antibody production is a compensatory mechanism stemming from the underlying T cell pathology. This sort of thing has been suggested vis a vis pathogen-specific antibodies by Naviaux IIRC.
If there are any active viruses, broad immunosuppression might be a bad idea.
Speaking of viruses, I'm still skeptical of this angle. The triggers are so heterogeneous for so many people, and most of the recent evidence points to viral exposures being no different for ME/CFS patients vs controls. I saw the recent post on EBV proteins in ME/CFS patients but the researchers did not establish whether that's causal or downstream from the immune dysfunction. My guess is the latter.
I wonder if IVIG at different doses could normalize an immune system that has both low total IgG and some bands of IgG that are high?
It might, but there have been cases where people get all their IgG removed via plasmapheresis and then IVIG replacement, and their disease persists. I don't think B cell dysfunction is at the root of this illness. Studies on IVIG have been contradictory, and there seems to be a subset for which the treatment is beneficial, but it's rarely curative. Even mainstream cutting-edge immunologists don't know how IVIG works for certain things, but it magically seems to induce Tregs and apoptosis of cytotoxic T cells. It can also be antiviral. I support its use in ME/CFS and would try it myself if I could afford it, but in 10 years I doubt it will be a common treatment for this disease.