Posts tagged: igg

Recurrent attacks of optic neuritis and myelitis are the hallmarks of both neuromyelitis optica (NMO) and multiple sclerosis (MS). NMO immunoglobulin G (NMO-IgG), which recognizes astrocytic aquaporin-4 (AQP4) water channels, is a specific serum autoantibody that distinguishes NMO from MS. The pathogenic role of the anti-AQP4 antibody (AQP4-Ab, NMO-IgG) in NMO has been speculated based on several studies in vitro.

Neuromyelitis optica (NMO) is an inflammatory autoimmune demyelinating disease of the central nervous system (CNS) which in autoantibodies produced by patients with NMO (NMO-IgG) recognize a glial water channel protein, Aquaporin-4 (AQP4) expressed as two major isoforms, M1- and M23-AQP4, in which the plasma membrane form orthogonal arrays of particles (OAPs). AQP4-M23 is the OAP-forming isoform, whereas AQP4-M1 alone is unable to form OAPs.

BACKGROUND: To establish whether or not multiple sclerosis (MS) and neuromyelitis optica (NMO) are different pathological entities, we wondered whether MS patients and NMO patients share the same pattern of human leukocyte antigen (HLA) predisposition. OBJECTIVE: To study a putative association between susceptibility to NMO and HLA class I or class II loci in Caucasians. METHODS: A total of 39 unrelated Caucasian patients with NMO and six patients at a high risk of converting to NMO were studied

BACKGROUND: Recently, a highly specific serum autoantibody was discovered in patients with neuromyelitis optica, called NMO-IgG, and aquaporin-4, the most abundant water channel in the CNS, was identified as the target antigen.

We report the case of a 60-year-old woman with myasthenia gravis (MG) and Basedow’s disease who seven years after thymectomy developed subacute myelitis, a limited form of neuromyelitis optica (NMO). The patient presented with a centrally located long spinal cord lesion (LCL) on cervical cord MRI, anti-aquaporin 4 (AQP4) antibody in serum, and HLA DPB1*0501

The clinical course of immune mediated optic neuritis (ON) will depend on the specific underlying inflammatory disease. These disorders have traditionally been classified according to clinical and MRI findings. Aquaporin-4 (AQP4) autoantibodies (neuromyelitis optica-IgG (NMO-IgG)) may have diagnostic and prognostic value in patients who present with isolated ON.

How high doses of intravenous IgG (IVIG) suppress autoimmune diseases remains unresolved. We have recently shown that the antiinflammatory activity of IVIG can be attributed to a minor species of IgGs that is modified with terminal sialic acids on their Fc-linked glycans.

In the past 10 years, neuromyelitis optica (NMO) has evolved from Devic’s categorical clinical description into a broader disease spectrum. Serum IgG antibodies have been identified in NMO patients with the water channel aquaporin-4 (AQP4) as their main target antigen.

OBJECTIVE: Neuromyelitis optica (NMO) is currently considered a severe relapsing CNS demyelinating disorder that is associated with aquaporin-4 immunoglobulin G (NMO-IgG) while in earlier reports of NMO in childhood it has been described as a benign and monophasic disorder. This study was performed to analyze the prevalence and the clinical course of NMO in a European pediatric cohort of patients with demyelinating CNS disorders

Background: Recurrent myelitis (rM) represents a pathogenetically heterogeneous group of inflammatory diseases with a selective involvement of the spinal cord. The recent description of NMO Ig-G antibody, the specific biomarker for Neuromyelites Optica (NMO), also in patients with recurrent myelitis with longitudinally extensive transverse spinal cord lesions (LETM), has brought to consider this disease an incomplete form of NMO (NMO Spectrum of Disorders). Methods: we retrospectively selected patients (pts) with rM attended our neurological department between January 2000 and March 2010

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.

Background: NMO-IgG autoantibody is now considered a useful serum biomarker of neuromyelitis optica (NMO). A series of clinical and pathological observations suggest that NMO-IgG may play a central role in NMO physiopathology. Objective: The aim of this in vitro-based study was to characterize molecular and functional consequences of interaction between NMO-IgG and primary cultures of astrocytes.