of the Max - MDC

Figure 1. Propidium iodide-fluorescence microscopy of the SJL mouse
living hippocampal brain slices without (upper left image) or with (lower
left image, with Fc control) the addition of PLP-specific encephalitogenic T
cells. As a positive control, the hippocampus is shown in response to application
of the neurotoxic agent NMDA (upper right image). Cell death induced
by encephalitogenic lymphocytes was reduced by soluble DR5:Fc (lower
right image). Scale bars 100 µm.
Figure 2. Reduced encephalitogenicity of TRAIL-deficient myelin-reactive
lymphocytes. MOG-specific lymphocytes from either TRAIL-deficient (ko) or wildtype
(wt) donors were transferred into wildtype recipients. Disease was significantly
milder in mice receiving TRAIL-deficient cells (black squares; n = 7), compared to
recipients of wildtype cells (white squares; n = 11; comparison of mean clinical
scores: F 10-49 (1,40) = 4.9, P < 0.05). Moreover, disease incidence was significantly
lower in mice receiving TRAIL-deficient lymphocytes (EAE manifestation, i.e. a
score of at least 1, was found in 1 out of 7 mice), as compared to recipients of
wildtype lymphocytes (EAE in 9 out of 11).
extensive transverse myelitis (LETM), corresponding to a
sensitivity of 62.8% and a specificity of 98.3%. By contrast,
Aqp-4 antibodies were virtually absent in 262 other participants,
which included patients with multiple sclerosis,
patients with other inflammatory and non-inflammatory
neurological diseases, patients with systemic autoimmune
diseases, and healthy controls. The newly developed assay
represents a highly specific, observer-independent, and
easily reproducible detection method facilitating clinically
relevant discrimination between NMO, MS, and other inflammatory
diseases. The challenge is now to unravel the role of
these antibodies and to discover the other targets in the
disease.
Selected Publications
Aktas, O, Smorodchenko, A, Brocke, S, Infante-Duarte, C,
Prozorovski, T, Meier, S, Osmanova, V, Kwidzinski, E, Pohl, E,
Beyer, M, Bechmann, I, Nitsch, R, Zipp, F. (2005) Neuronal
damage in autoimmune neuroinflammation mediated by the
death ligand TRAIL. Neuron. 46, 421-432.
Infante-Duarte, C., A. Weber, J. Krätzschmar, T. Prozorovski, S.
Pikol, J. Bellmann-Strobl, O. Aktas, J. Dörr, J. Wuerfel, C.-S.
Stuerzebecher, F. Zipp. (2005) Frequency of blood CX3CR1-positive
natural killer cells correlates with disease activity in multiple
sclerosis patients. The FASEB Journal. 19: 1902-1904.
Zipp, F, Aktas, O. (2006) The brain as a target of inflammation:
common pathways link inflammatory and neurodegenerative
diseases. Trends Neurosci. 29, 518-527.
184 Function and Dysfunction of the Nervous System