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Multiple sclerosis (MS) is an inflammatory T cell-mediated disease of the central nervous system (CNS) (1). It is characterized by focal demyelination and axonal loss leading to a range of symptoms including decline in motor function and sense perception (2). In PNAS, Sabatino et al. (3) further shed light on the underlying mechanism of current MS therapies.In mice, MS can be modeled by immunization with myelin-derived antigens, leading to a disease termed experimental autoimmune encephalomyelitis (EAE) (4). Many studies have defined the cells that are important in the activation of the T cells involved in EAE (5) as well as the role of the T cells involved in disease pathogenesis (6). In humans, neither a definite genetic nor environmental cause has been defined, nor has a cure been discovered for MS (7). Nevertheless, genetic studies have shown that genes of the immune system are highly associated with disease development (8). Importantly, one … [↵][1]1To whom correspondence may be addressed. Email: waisman{at}uni-mainz.de. [1]: #xref-corresp-1-1

Unraveling the T–B tangle in anti-CD20 multiple sclerosis therapy