Rich, as far as I know, it goes like this: Bcells go through natural selection in the body. Even given the same stimulus exactly, they also seem to have some kind of internal tendencies, as to what role they will exactly play. In any case, in the IgM form they have five places to bind, they are rough and ready so to speak, in responding to an antigen. They bind to it but imperfectly. IE there are classes of bcells, ready to do their best, to bind roughly but strongly (five places) to an antigen. Then they these active bcells compete against each other, in successive generations in a form of evolution and natural selection, shuffling genes and refining binding until one emerges with a really really good fit. The tcells approve that one to clonally expand. It goes into the bone marrow becoming a long lived plasma cell (I'm pretty sure--it's been over a month since I looked at this stuff). It clonally expands, and at that point, your fever breaks, so to speak. You've got zillions of IgG antibodies, bcells generating antibodies in the dimer form, with a nearly exquisite specificity for the antigen. And you get over your flu and that bug never bugs you again. Anyway, the plasma cells can regenerate the bcells, they are long lived, for at least ten years in the bone marrow. So when you deplete circulating bcells, and the antibodies they made gradually fall away, you get temporary recovery from the CNS autoimmune disease known as ME/CFS. But eventually the plasma cells create a new generation of bcells. Most of the time, at that point, the disease returns. And you have to re-treat. Therefore, the idea that at that point, glutathione is normal because inflammation and oxidative stress is down, doesn't make sense to me. I suggest before trying to fit it into or out of your theory, that you go and read a lot of Jonathan Edwards' work, and then Fluge & Mella's view--have you read the actual studies? If not you are free to email me and I can forward you some good stuff for you to chew your noggin' on. It doesn't seem you may have delved into this enough, and into the history of bcell depletion and Rituximab, to necessarily understand all the details. Not trying to sound annoying at all...just trying to help.