The good news that anti-CD20 is affecting relapsing and progressive MS is going to mean a rethink.
Anti-CD20 inhibits many suspected autoimmunities. Is it by depleting a CD20+ T cell, blocking antigen presenting function or by killing the reservoir of the autoimmune virus that leads to MS.
The concept of autoimmunity has been led by T cell immunologists, and some have B cells and antibodies at their core despite being driven by T cells.
Personally I think that anti-CD20 is pretty rubbish in EAE, as this is a T cell-mediated disease and the effects of B cell depletion is marginal.
Rituximab was good at inhibiting EAE in human CD20-transgenic mice, it was also killing T cells as well as B cells in the mice.
However, we will now see EAE become a B cell-mediated disease.
Copaxone will get another mechanism of action:-)...but it is potentially an antigen presentation blocker anyway
At TeamG, we left the focus of T cells many years ago, although recently we have been there and EAE can be used to model damage and disease control irrespective of whether it is T cell mediated or not...however is this another nail in the coffin?