Hello everyone, we are having an interesting discussion in another thread about the question if it makes sense to try Rituximab even if you don't have any known autoantibodies. Rituximab is known to help for autoimmune diseases like rheumatoid arthritis and lupus erythematosus, and there is anecdotal evidence in this forum of people with autoimmunity problems who benefitted substantially from it (most prominently Gingergrrl). BUT: As far as I know, the Norwegian trials have never established a link between existing autoimmune disease and response to Rituximab. In their very first trial, one of the three major responders had no known autoimmune disease: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC2711959/ It may well be that all patients who responded had autoimmune disease of an unknown and undiscovered kind. Or Rituximab might work for other reasons in patients without autoimmunity. Maybe the problem isn't autoantibodies, but overproduction of "normal" antibodies that cause harm to the body. Such antibodies are known to exist, e.g., the anti-streptolysin antibody is against streptococcal bacteria (so not an autoantibody), but it also attacks body tissues that have a similar protein. Prof. Edwards once surmised that Rituximab might work by stopping overproduction of one or several low-affinity/broad spectrum antibody that aren't actually autoantibodies. And there has always been the hypothesis that Rituximab works in some patients simply by killing Epstein Barr Virus, whose main reservoir are the B-cells. In any of these cases, patients whose autoimmune panel is negative would have a chance to be responders and, again, the Norwegian researchers have not established a link between autoimmunity and response to Rituximab although this is their main hypothesis of how Rituximab works (so it's probably not because they haven't looked into this). I am very curious to hear your opinions!