![]() It took 2 years for her to find the right diagnosis and due to a lack of aggressive treatment, she lost the sight in both of her eyes. In parallel, they are screening for novel antibodies to glial cells in related disorders such as encephalitis and optic neuritis.Īndrea Mitchell has had relapsing form of MOG-AD since October 2011. Biomarker assays for other autoimmune diseases of the central nervous system: They are developing assays that detect autoreactive T cells in NMO and MOG antibody disease. In addition to understanding why and how these T cells are involved in MOG antibody disease, they are developing a treatment to target these cells.Ĥ. These specialize T cells react to MOG in mouse models and attack the central nervous system. The immunopathogenesis of MOG antibody disease: This may depend on a subset of T cells called gamma/delta T cells. To understand how this gene is involved in this immune process, they generated a mouse model with this mutation.ģ. Genetic basis of transverse myelitis: His team discovered a genetic mutation in VPS37a found in a group of patients with a familial form of transverse myelitis (TM). Now, they are using this mouse model to create a tolerization therapy to desensitize the immune response to aquaporin-4.Ģ. Development of animal models of neuromyelitis optica (NMO) with the goal of tolerization as a sustainable long term treatment: His team generated a mouse model of NMO based on pathogenic T cells reactive against the aquaporin-4 water channel. Levy’s research focuses on four main areas:ġ.
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