Twenty-seven treatment-naïve patients with relapsing-remitting multiple sclerosis (MS) and 13 with neuromyelitis optica spectrum disorder (NMOSD) were enrolled during a time of acute flare-up. Common cerebrospinal fluid (CSF) features were increased CD29- and/or CD45RO-positive helper T cells capable of propagating inflammation in the central nervous system (CNS). B cell activation in the CSF was unique to MS, while an increase in CD4CD192 (CCR2) cells in blood and breakdown of the blood-brain barrier (BBB) characterized NMOSD. Intravenous corticosteroid therapy suppressed neuroinflammation via modulation of cellular immunity in MS, as opposed to restoration of the BBB in NMOSD.
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