Imaging Immune-Mediated Depression and Cognitive Impairment in Autoimmune Neurologic Diseases: MRS of Patients with Multiple Sclerosis and Transverse Myselitis Adam I. Kaplin, M.D., Ph.D.
Anti–Aquaporin-4 monoclonal antibody blocker therapy for neuromyelitis optica Lukmanee Tradtrantip PhD 1 , Hua Zhang PhD 1 , Samira Saadoun PhD 2 , Puay-Wah Phuan PhD 1 , Chiwah Lam BS 3 , Marios C.
We reported recently that intracerebral administration of NMO-IgG with human complement produces neuromyelitis optica (NMO) lesions in mice. We examined the role of T cells in the formation of NMO lesions by comparing brain histopathology in wildtype and nude mice. Brains were co-injected with IgG from NMO patients and human complement.
A multi-institutional research team has found that rare variants in the gene coding an enzyme that controls the activity of a key immune cell occur more frequently in individuals with autoimmune disorders like rheumatoid arthritis and type 1 diabetes. Their report, which will appear in the journal Nature and is receiving early online release, identifies a pathway that could be a therapeutic target and may present a model for future investigations of the role of rare gene variants in common disorders.
Objective: Clinical studies indicate that anti-CD20 B-cell depletion may be an effective multiple sclerosis (MS) therapy. We investigated mechanisms of anti-CD20-mediated immune modulation using 2 paradigms of experimental autoimmune encephalomyelitis (EAE). Methods: Murine EAE was induced by recombinant myelin oligodendrocyte glycoprotein (rMOG), a model in which B cells are considered to contribute pathogenically, or MOG peptide (p)35-55, which does not require B cells.
Background and Goals: Neuromyelitis optica (NMO) is associated with aquaporin-4 (AQP4)-specific IgG1 antibodies. Human IgG1 is a T cell-dependent antibody subclass, which suggests that AQP4-specific T cells may participate in NMO pathogenesis, a possibility also supported by observations that AQP4-specific antibodies are pathogenic only in the presence of CNS inflammation. We have been studying T cell recognition of AQP4 in NMO patients and in mice in order to understand the potential role of T cells in NMO pathogenesis and to develop a model of NMO.