Isn't MS usually considered a T-cell mediated disease? Or do you think this interpretation is incorrect, akin to those chasing after T-cells in RA? How about the seronegatives and IBD (which of course are not antibody mediated)? The latter at least seem to be IL-17 driven, given the success so far of secukinumab (phase 3 trial published recently - looked good) and ustekinumab. Perhaps autoantibodies in MS though are a secondary phenomenon?
The evidence that MS is more likely B-cell mediated (or has a mostly B-cell driven mechanism) has been growing since 2008.
In 2008 Stephen Hauser from UCSF published the landmark study in NEJM, results of a phase II clinical trial of rituximab in relapsing-remitting MS (RRMS), showing very impressive efficacy.
B-Cell Depletion with Rituximab in Relapsing–Remitting Multiple Sclerosis
This was so revolutionary because it was the first evidence challenging the then current dogma that MS was definitely a T-cell mediated disease, it's not.
MS research really shifted after this. The only reason you don't see rituximab as an FDA-approved drug for RRMS today is because of standard pharmaceutical industry evil behavior. Roche/Genentech knew that rituximab would be at the end of its patent when a phase III trial completed and they refused to fund any phase III trial. Instead they made the medical community completely start the process over with their new 3rd gen CD20 drug ocrelizumab. The OPERA I and II phase III trial results of ocrelizumab in RRMS and secondary-progressive MS (SPMS) should be published soon, preliminary results showed almost identical efficacy to rituximab. But as of today there still is no FDA-approved CD20 drug for MS where if they went forward with rituximab it would've been approved and in use for a while now.
While rituximab was not so effective in primary progressive MS (PPMS), a more severe version of the disease, that did not mean that PPMS didn't have a very significant B-cell mediated component. In fact the 3rd gen ocrelizumab is the first drug shown to be effective in PPMS, preliminary results of the ORATORIO trial should also be published soon. In fact to me PPMS is a great example where rituximab doesn't work but the B-cell hypothesis is not wrong because the more potent ocrelizumab has much better efficacy. We should keep this example in mind when people challenge that rituximab doesn't work in a subset of PWME because they think they don't have the same disease (e.g. chronic infection) when in fact it could just mean that rituximab is less effective in this cohort for as yet unknown reasons.
A good blog post on the history of rituximab in MS here:
The Shameful Story of Rituximab in Multiple Sclerosis