Posts tagged: cells

Evaluation of a Multiparametric Immunofluorescence Assay for Standardization of Neuromyelitis Optica Serology Letizia Granieri,#1,2,* Fabiana Marnetto,#1,2 Paola Valentino,1,2 Jessica Frau,3 Agata Katia Patanella,4 Petra Nytrova,5 Patrizia Sola,6 Marco Capobianco,1 Sven Jarius,7 and Antonio Bertolotto1,2 Author information ? Article notes ? Copyright and License information ? Go to: Abstract.

Original Article Neuromyelitis optica IgG does not alter aquaporin-4 water permeability, plasma membrane M1/M23 isoform content, or supramolecular assembly Andrea Rossi1,2, Julien Ratelade1,2, Marios C. Papadopoulos3, Jeffrey L.

Notable Increased Cerebrospinal Fluid Levels of Soluble Interleukin-6 Receptors in Neuromyelitis Optica. Wang H, Wang K, Zhong X, Dai Y, Qiu W, Wu A, Hu X.

Devic’s syndrome was first described in 1870 by Sir Thomas Allbutt (what a name to have had as a kid!) who pointed out an association between myelitis and optic nerve disorder.? In 1894, Eugene Devic and his student Fernand Gault described 16 patients who had lost vision in one or both eyes and developed spastic weakness, sensory loss, and incontinence.? The other name of the condition was neuromyelitis optica (NMO). A major breakthrough came in 2004 when a specific marker NMO-IgG was found for the disorder [1].? IgG stands for immunoglobulin (a kind of antibody).

A surprising discovery about the complex make-up of our cells could lead to the development of new types of medicines, a study suggests.

Autoantibodies against astrocyte water channel aquaporin-4 (AQP4) are highly specific for the neuroinflammatory disease neuromyelitis optica (NMO). We measured the binding of NMO autoantibodies to AQP4 in human astrocyte-derived U87MG cells expressing M1 and/or M23 AQP4, or M23 mutants that do not form orthogonal array of particles (OAPs).

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.

There are several molecular entities common to the immune and nervous systems. Salient among them are the chemokines and their receptors, which play remarkably varied and potent roles in immunobiology and neurobiology

The plasma membrane assembly of aquaporin-4 (AQP4) water channels into orthogonal arrays of particles (OAPs) involves interactions of AQP4 N-terminal domains. To study in live cells the site of OAP assembly, the size and dynamics of plasma membrane OAPs, and the heterotetrameric associations of AQP4, we constructed green fluorescent protein (GFP)-labeled AQP4 “long” (M1) and “short” (M23) isoforms in which GFP was inserted at the cytoplasm-facing N or C terminus or between Val-141 and Val-142 in the second extracellular loop of AQP4. The C-terminal and extracellular loop GFP insertions did not interfere with the rapid unrestricted membrane diffusion of GFP-labeled M1 or the restricted diffusion and OAP assembly of GFP-labeled M23

We evaluated 30 patients with clinically definite multiple sclerosis (MS) and 8 patients with neuromyelitis optica (NMO) to investigate correlations between Th1/Th2 balance, disease activity, effects of interferon (IFN)-beta treatment, and expressions of chemokine receptors CXCR3 and CCR4 on CD4+ and CD8+ T cells in peripheral blood. MS and NMO patients in the relapsing phase showed a significantly increased CD4+CXCR3+/CD4+CCR4+ ratio and CD8+CXCR3+/CD8+CCR4+ ratio compared with respective patients in the remission phase

BACKGROUND: Neuromyelitis optica (NMO), a severe demyelinating disease, represents itself with optic neuritis and longitudinally extensive transverse myelitis. Serum NMO-IgG autoantibodies (Abs), a specific finding in NMO patients, target the water channel protein aquaporin-4 (AQP4), which is expressed as a long (M-1) or a short (M-23) isoform.

In order to clarify the immunological characteristics of multiple sclerosis (MS) and neuromyelitis optica (NMO), we analyzed CD3, CD4, CD8, CD20, CD4(+)CD25(+), CD4(+)CD29(+), and CD8(+)CD11a(high) cells in peripheral blood from patients with MS (16 stable, 6 active) and NMO (15 stable, 7 active), as well as 9 with NMO spectrum, 6 with clinically isolated syndrome (CIS), and 13 with other neurological diseases using flow cytometry. Significant decreases in the numbers of CD8(+) CD11a(high) cells were observed in stable and active MS and CIS