Aquaporin 4-specific T cells in neuromyelitis optica exhibit a Th17 bias and recognize Clostridium ABC transporter. Varrin-Doyer M, Spencer CM, Schulze-Topphoff U, Nelson PA, Stroud RM, C Cree BA, Zamvil SS.
Neuromyelitis optica (NMO) is an inflammatory demyelinating disease that predominantly affects the optic nerves and spinal cord. Recombinant antibodies (rAbs) generated from clonally expanded plasma cells in an NMO patient are specific to AQP4 and pathogenic. We screened phage-displayed peptide libraries with these rAbs, and identified 14 high affinity linear and conformational peptides
Neuromyelitis optica (NMO) is an autoimmune demyelinating disease characterized by the presence of anti-aquaporin-4 (AQP4) antibodies in the patient sera. We recently reported that these autoantibodies are able to bind AQP4 when organized in the supramolecular structure called the orthogonal array of particles (OAP).
The autoantibody to aquaporin-4 (AQP4) is a marker and a pathogenetic factor in Neuromyelitis Optica (NMO) (Devic’s syndrome). Our aim was to identify B-cell antigenic linear epitopes of the AQP4 protein and investigate similarities with other molecules. To this end, we screened sera from 21 patients positive for anti-AQP4 antibodies (study group), from 23 SLE and 23 pSS patients without neurologic involvement (disease controls) and from 28 healthy individuals (normal controls)
Neuromyelitis optica is an autoimmune demyelinating disease characterized by the presence of anti aquaporin-4 (AQP4) antibodies in the patient sera.
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.