 Multiple sclerosis, MS, is believed to be a CD4 T-cell mediated autoimmune disease. However, many current MS treatments, believed to act via T-cell inhibition, also depleted CD19+, CD27+, memory B-cells. This depletion was substantial and long-term following CD52 and CD20th depletion, and both induced long-term inhibition with few treatment cycles. Importantly, memory B-cells were augmented by B-cell activating factor, a tassecept, and tumor necrosis factor, infliximab, which are known to worsen MS. This creates a unifying concept centered on memory B-cells that is consistent with therapeutic, histopathological and etiological aspects of MS. This article was authored by David Baker, Monica Marta, Gareth Price, and others.