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Posts tagged: inflammatory

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.


Low Serum Vitamin D Levels and Recurrent Inflammatory Spinal Cord Disease Maureen A.


Pathogenic T cell responses against aquaporin 4. Pohl M , Fischer MT , Mader S , Schanda K , Kitic M , Sharma R , Wimmer I , Misu T , Fujihara K , Reindl M , Lassmann H , Bradl M . Source Department of Neuroimmunology, Center for Brain Research, Medical University Vienna, Spitalgasse 4, 1090, Vienna, Austria.


Beneficial Plasma Exchange Response in Central Nervous System Inflammatory Demyelination Setty M. Maga?a, BS; B.


Research Anti-CD20 B-cell depletion enhances monocyte reactivity in neuroimmunological disorders Klaus Lehmann-Horn , Eva Schleich , Deetje Hertzenberg , Alexander Hapfelmeier , Tania Kuempfel , Nikolas von Bubnoff , Reinhard Hohlfeld , Achim Berthele , Bernhard Hemmer and Martin S Weber ? For all author emails, please log on . Journal of Neuroinflammation 2011, 8 :146? doi:10.1186/1742-2094-8-146 Published: 26 October 2011 Abstract (provisional) Background Clinical trials evaluating anti-CD20-mediated B-cell depletion in multiple sclerosis (MS) and neuromyelitis optica (NMO) generated encouraging results.


Multiple sclerosis is an inflammatory demyelinating disorder of the CNS. Recent studies have suggested diverse mechanisms as underlying demyelination, including a subset of lesions induced by an interaction between metabolic insult to oligodendrocytes and inflammatory mediators


Interleukin-17 (IL-17) secreted by T helper 17 (Th17) cells is essential in the development of experimental autoimmune encephalomyelitis (EAE). However, it remains unclear how IL-17-mediated signaling in different cellular compartments participates in the central nervous system (CNS) inflammatory process.


Inflammatory lesions in the central nervous system of patients with neuromyelitis optica are characterized by infiltration of T cells and deposition of aquaporin-4-specific antibodies and complement on astrocytes at the glia limitans. Although the contribution of aquaporin-4-specific autoantibodies to the disease process has been recently elucidated, a potential role of aquaporin- 4-specific T cells in lesion formation is unresolved. To address this issue, we raised aquaporin-4-specific T cell lines in Lewis rats and characterized their pathogenic potential in the presence and absence of aquaporin-4-specific autoantibodies of neuromyelitis optica patients


The glial water channel aquaporin-4 (AQP4) is implicated in the control of ion and osmohomeostasis in the sensory retina. Using retinal slices from AQP4-deficient and wild-type mice, we investigated whether AQP4 is involved in the regulation of glial cell volume under altered osmotic conditions.


Neuromyelitis optica (NMO) is an inflammatory disease mainly affecting the optic nerve and spinal cord.


There is a complex, diverse array of “preceding environmental events” and perhaps unconnected immune-related events which are often associated with the period before patients are diagnosed with NMO. In this review we discuss in detail how the different isoform structures of AQP4 in different membrane locales and in different cell types might be related to pathology. Changes in AQP4 expression in CNS and non-CNS tissue can be regulated by inflammatory mediators induced during and following infection or by underlying autoimmunity and can result in the induction of AQP4-specific lymphocytes and ensuing pathogenesis.


The detection of antibodies against aquaporin-4 (AQP4) has improved the diagnosis of neuromyelitis optica (NMO). We evaluated a recently established cell-based anti-AQP4 assay in 273 patients with inflammatory CNS demyelination. The assay had a specificity of 99% and a sensitivity of 56% to detect all NMO patients and of 74% to detect the recurrent NMO patients, similar to the initial studies reported.