BBA Clin. 2015 Jan 15;3:126-34. doi: 10.1016/j.bbacli.2015.01.003. eCollection 2015. Kariya Y1, Kariya Y1, Saito T1, Nishiyama S2, Honda T3, Tanaka K4, Yoshida M5, Fujihara K2,…
Clinical Usefulness of Cell-based Indirect Immunofluorescence Assay for the Detection of Aquaporin-4 Antibodies in Neuromyelitis Optica Spectrum Disorder Eun-suk Kang, M.D.,1 Ju-Hong Min, M.D.,2 Kwang Ho Lee, M.D.,2 and Byoung Joon Kim, M.D.2 Author information ? Article notes ? Copyright and License information ? Go to: Abstract. Background The presence of antibodies to aquaporin-4 (AQP4) has been identified as a key characteristic of neuromyelitis optica spectrum disorder (NMOSD), an autoimmune inflammatory demyelinating central nervous system (CNS) disorder. We evaluated the performance of a cell-based indirect immunofluorescence assay (CIIFA) for detecting AQP4 antibodies using antigen prepared with a recombinant AQP4 peptide transfection technique and assessed the usefulness of CIIFA for diagnosis of NMOSD in routine clinical practice.
Diagnostic utility of NMO/AQP4-IgG in evaluating CNS inflammatory disease in Thai patients. Apiwattanakul M, Asawavichienjinda T, Pulkes T, Tantirittisak T, Hemachudha T, Horta ES, Jenkins SM, Pittock SJ. Source Department of Neurology, Prasat Neurological Institute, Bangkok, Thailand
Cerebrospinal fluid B-cell expansion in longitudinally extensive transverse myelitis associated with neuromyelitis optica immunoglobulin G. Dale RC, Tantsis E, Merheb V, Brilot F. Source Neuroimmunology Group, Institute of Neuroscience and Muscle Research, The Children’s Hospital at Westmead, University of Sydney, Sydney, NSW, Australia
Beneficial Plasma Exchange Response in Central Nervous System Inflammatory Demyelination Setty M.
Beneficial Plasma Exchange Response in Central Nervous System Inflammatory Demyelination Setty M. Maga?a, BS; B.
Damage to the central nervous system can often result from the progression of an autoimmune disease. Demyelination often occurs as a result, where the myelin sheath on a neuron’s axons is destroyed due to excessive autoimmune responses (1).This destruction ultimately leads to lesions in the brain or spinal cord (2,3).The uncontrolled autoimmune responses can be primary, where the infiltrates begin the destruction of the myelin sheath, or secondary, where infiltrates respond to previous CNS damage and subsequently further the damage (4) . Multiple Sclerosis (MS) is the most noted example of a CNS demyelinating autoimmune disease (3,4), with 350,000-500,000 individuals currently diagnosed(3)
The central nervous system ( CNS ) represents the largest part of the nervous system , including the brain and the spinal cord . Together with the peripheral nervous system , it has a fundamental role in the control of behavior
Aquaporin-4 (AQP4) deficiency in mice reduces neuroinflammation in experimental autoimmune encephalomyelitis (EAE) produced by active immunization with myelin oligodendrocyte glycoprotein peptide (MOG).
The functional role of ELR-positive CXC chemokines in host defense during acute viral-induced encephalomyelitis was determined. Inoculation of the neurotropic JHM strain of mouse hepatitis virus (JHMV) into the central nervous system (CNS) of mice resulted in the rapid mobilization of PMNs expressing the chemokine receptor CXCR2 into the blood. Migration of PMNs to the CNS coincided with increased expression of transcripts specific for the CXCR2 ELR-positive chemokine ligands CXCL1, CXCL2, and CXCL5 within the brain.
Increased blood-brain barrier (BBB) disruption can be found in patients with neuromyelitis optica (NMO); however, its clinical implication and association with disability at acute attack remains obscure. The purpose of the study was to evaluate the clinical significance of BBB disruption and the subsequent cerebrospinal fluid (CSF)/serum IgG gradient in NMO.
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.