Dissecting Neuromyelitis optica (NMO), an autoimmune disease of the CNS
We study NMO, a severe inflammatory disease of the central nervous system (CNS), which is characterized by the formation of large astrocyte-destructive lesions, mostly in the spinal cord and in the optic nerves of affected patients. Most patients harbor pathogenic auto-antibodies, the so-called NMO-IgGs, in their serum. These antibodies are directed against the water channel aquaporin 4 (AQP4), which is found on astrocytes in the CNS. When these antibodies gain access to the brain, they bind to AQP4 on the surface of astrocytes and initiate complement-mediated, antibody-dependent destruction of these cells. Subsequently, myelin loss ensues. We currently dissect the role of T cells, antibodies and cytokines in lesion formation. Recent findings and highlights of current research are outlined below:
1. Highly pathogenic AQP4-specific T cells and NMO-IgG determine size and location of astrocyte-destructive lesions.
Paper: Zeka et al., (2015), Acta Neuropathol, DOI 10.1007/s00401-015-1501-5
PhD students: Bleranda Zeka, Maria Hastermann
Master student: Nikolaus Kögl
Student coworker: Nathalie Kaufmann
2. T cells specific for other CNS antigens can also initiate NMO-like lesions in the presence of NMO-IgG, provided that these T cells are activated and upregulate the activation marker OX40.
Paper: Pohl et al., (2013), Acta Neuropathologica Communications 1:85
PhD students: Maria Pohl, Maja Kitic, *Joana Machado-Santos (*PhD student of Prof. Lassmann)