A dual role of B cells in experimental autoimmune encephalomyelitis (EAE), the animal model of the human autoimmune disease multiple sclerosis
(MS), has been established. In the first role, B cells contribute to
the pathogenesis of EAE through the production of anti-myelin antibodies
that contribute to demyelination. On the contrary, B cells have also
been shown to have protective functions in that they play an essential
role in the spontaneous recovery from EAE. In this review, we summarize
studies conducted in a number of species demonstrating the conditions
under which B cells are pathogenic in EAE. We also discuss the phenotype
and anti-inflammatory mechanisms of regulatory B cells.
This all well and good, but you need these reviews BEFORE the human trials are done. It has already been shown that rituximab and ocreluzimab (B cell blocking agents) can inhibit some aspects of MS whilst Atacicept another B cell blocking agent makes MS worse. My old Boss (John Leslie Turk) reported on B regulatory cells probably long before the above authors were born. That work was forgotten but the potential can come back to bite you in the a**e (a*s in American). Do anti B cell agents work by blocking anti-body production (immunologists view), but what about blocking antigen presentation function (alternative immunologist view) of if you are Prof B viral infection of B cells. It is again a case of the tail wagging the dog. The effects in EAE (speaking as an EAEer) are kind of irrelevant when we know what is going on in humans....but do we know what is going on? We need EAEers to change views before they they are shown to be wrong not after, otherwise it is just more and more bad science and importantly more false hopes for MSers.