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Immunoregulatory Neuroprotection of Cerebral Ischaemia
Conclusion reduced, resulting in neuroprotection. The response of the immune
Cerebral ischaemia first is a local event in the brain, but has strong system – peripheral and central immune activation followed by
secondary systemic effects on the whole organism. The attenuation of peripheral immunoexhaustion – should be considered an important
the peripheral immune response after ischaemia has been target in stroke therapy. n
underestimated for many years. Cerebral ischaemia induces strong
immune activation in the spleen followed by delayed immuno-
suppression. Within 24 hours after cerebral ischaemia, splenocytes
Sönke Schwarting is a Medical Resident in the
upregulate chemokine receptors and pro-inflammatory cytokines, which
Department of Neurology at the University of
Heidelberg in Germany. His clinical interests include a
support their recruitment to the ischaemic brain lesion. Post-ischaemic broad spectrum of neurological disorders and his
neurodegeneration is partly mediated by these recruited immune cells.
scientific research focuses on stroke medicine,
Data from stem and precursor cell transplantation experiments show
including experimental as well as clinical studies.
Dr Schwarting has a specific interest in stem cell
strong immunoregulatory activity and interference with the early post- therapeutic approaches in cerebral stroke.
ischaemic immune activation of the spleen. Transplanted stem and
precursor cells are detected substantially within the spleen. They
Harald Neumann is a Professor of Neural Regeneration at the Institute of
attenuate splenic pro-inflammatory activity and chemokine receptor Reconstructive Neurobiology of the University Hospital Bonn in Germany. His research
expression after cerebral ischaemia. Consequently, due to stem and
interests include neuroinflammatory diseases and investigation of microglia function
mechanisms in neuroinflammation and neuroregeneration.
precursor cell treatment, a lower number of immune cells become
recruited to the ischaemic lesion site and post-ischemic inflammation is
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