Simon M, et al. - Researchers sought to gain in-depth understanding of the effects of anti-CD52 antibody treatment on the B cell compartment in the central nervous system (CNS) by using myelin basic protein (MBP)-proteolipid protein (PLP)-induced experimental autoimmune encephalomyelitis (EAE) in C57BL/6 (B6) mice as B cell-dependent model of multiple sclerosis (MS). Findings revealed that the administration of anti-CD52 antibody only at the peak of disease resulted in attenuated EAE. While the production of MP4-specific IgG remained unaffected, CNS infiltrates and B cell aggregates were almost completely depleted, even when the treatment was given as late as 60 days after onset. Overall, they concluded that anti-CD52 treatment abrogated B cell infiltration and disrupted existing B cell aggregates in the CNS.