Abstract
Multiple sclerosis (MS) is considered an immunopathological neurodegenerative illness, the pathogenesis of which mainly depends on abnormally polarized T-lymphocytes of the Th1 and Th17 subsets. It has been shown recently, especially in clinical trials proving the clinical effectiveness of antibodies aiming at the CD20 antigen, specifically present on mature B-lymphocytes only, that B-lymphocytes also are an integral part of the destructive inflammation in MS.
These lymphocytes may produce autoantibodies which, after establishing a link with CNS structures, can become responsible for their damage through activation of the complement of through phagocytosis. First of all, however, B-lymphocytes are cells capable of very potent antigen presentation to T-lymphocytes, thus inducing their abnormal functional polarization.
The number of activated B-lymphocytes is increased in the brain parenchyma of MS patients. In patients with primary progressive MS, tertiary lymphoid structures were found in the meninges, formed mostly by B-lymphocytes.
Ample clinical experience with the application of biological anti-CD20 therapy in other indications shows that both immediate and long-term clinical effect of this therapy depends on unique characteristics on individual antibodies used. Ocrelizumab seems to be irreplaceable for MS patients from this point of view.