Brain, Vol. 125, No. 1, 75-85, January
Christine Stadelmann (1), Martin Kerschensteiner (2,3), Thomas Misgeld (2,3), Wolfgang Brück (1), Reinhard Hohlfeld (2,3) and Hans Lassmann (4)
(1) Institute for Neuropathology, Charité, Humboldt-University, Berlin,
(2) Institute for Clinical Neuroimmunology, Klinikum Grosshadern, Ludwig-Maximilians-University, Munich,
(3) Department of Neuroimmunology, Max-Planck-Institute for Neurobiology, Martinsried, Germany and
(4) Department of Neuroimmunology, Brain Research Institute, University of Vienna, Austria
Recent immunohistological and imaging studies emphasize the crucial role of axonal injury in determining the extent of permanent neurological deficits in patients with multiple sclerosis.
We have recently shown that human immune cells are capable of producing the neurotrophin brain-derived neurotrophic factor (BDNF), which can prevent axonal and neuronal damage after various pathological insults.
BDNF imported into the CNS by immune cells would thus be an attractive candidate for mediating neuroprotective effects in multiple sclerosis.
The aim of the present study was to perform a detailed immunohistochemical analysis of the expression of BDNF and its receptor truncated trkB tyrosine kinase receptor (gp145trkB) in a series of multiple sclerosis brain lesions.
Our data show that various types of neurones throughout the brain are BDNF immunopositive in multiple sclerosis patients as well as in controls. Furthermore, in multiple sclerosis lesions, BDNF is primarily present in immune cells (T cells, macrophages/microglia) and reactive astrocytes.
The number of BDNF immunopositive cells correlates with lesional demyelinating activity.
The BDNF receptor gp145trkB is found in neurones in the immediate vicinity of multiple sclerosis plaques as well as in reactive astrocytes within the lesion, but not in immune cells.
Our results demonstrate that both BDNF and gp145trkB are expressed in multiple sclerosis lesions.
This suggests that BDNF and gp145trkB
are involved in immune-mediated neuroprotective interactions in multiple
sclerosis, and supports the concept that immune cells produce both damaging
and protective factors in multiple sclerosis lesions.
Copyright © 2002 Oxford University
Copyright © 2002 Oxford University Press