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Clinician Scientist Group on Stroke-Immunology

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Our group is interested in the interplay between the brain and the immune system after an acute stroke. An acute lesion of the brain disturbs the well-balanced interconnection between both systems. Thereby our research focuses on both directions of brain-immune interaction: 1) The impact of immune mechanisms on neuronal damage and recovery after stroke and 2) systemic immunomodulation and infectious complications after acute brain injury. Our group has a strong translational interest with the ultimate goal of developing new concepts and potential therapies for the benefit of stroke patients.

Our methodical spectrum covers diverse brain ischemia models, transgenic animal models, a broad spectrum of cutting-edge immunological techniques as well as histological, biomolecular and behavioral analysis tools. Because of our inter-disciplinary research approach we are highly connected with local and international collaborators.

We are currently focusing on the following research goals:

Project 1: Immune mechanisms of endogenous neuroprotection

Among many detrimental cascades, inflammatory mechanisms have come into the focus of current research because they contribute substantially to secondary brain damage. Neuroinflammation after stroke results in collateral damage to tissue that might be rescued in a prolonged time window after ischemia onset. On the other hand, immunological reactions after tissue damage are tightly controlled by active regulatory mechanisms. We have previously identified an important neuroprotective role of endogenous regulatory T cells in stroke (Liesz et al., Nature Medicine, 2009). Use of this potent endogenous mechanism by directly augmenting their immunosuppressive capacities or their downstream signalling pathways is being tested as promising therapeutic targets at the center of post-ischemic neuroinflammation.








Planas AM, comment on Liesz et al., Nature Medicine, 2009


Project 2: Leukocyte-endothelial interaction in acute stroke

A key mechanism of post-stroke neuroinflammation is migration of pro-inflammatory leukocytes to the ischemic brain (Liesz et al., Brain, 2011). Brain invading leukocytes are activated upon brain invasion and are major producers of neurotoxic cytokines in ischemic as well as hemorrhagic brain lesions (Liesz et al., PlosOne, 2011 and J Neuroimmunol 2013). The critical step in leukocyte invasion to the damaged brain after stroke is their interaction with endothelium at the migration site. The goal of this project is to further characterize the highly complex leukocyte-endothelial interplay after stroke and define new targets to specifically inhibit invasion of neurotoxic leukocyte subpopulations.






A) Brain-invading T cells (CD3) co-localize with active endothelium at the ischemic border zone. B) Blocking the Integrin CD49d by monoclonal antibodies effectively reduces the invasion of various leukocyte subpopulations (Liesz et al., Brain, 2011).


Project 3: DAMPs in post-stroke systemic immunomodulation

Infectious complications are a leading cause of morbidity and mortality after stroke. A stroke-induced immunosuppression syndrome (SIDS) has been identified as a major risk factor for post-stroke infectious complications (Dirnagl et al., Stroke, 2007). Lymphocytopenia and reduced lymphocyte and monocyte function are the hallmarks of this syndrome (Hug*, Liesz* et al., Stroke, 2011). These effects depend on lesion size and were observed mainly after large ischemic stroke (Liesz et al., Stroke, 2009). However, the pathophysiological link between brain lesion and systemic immune changes is still unclear. The aim of this project is to characterize humoral mediators which are released by the necrotic brain tissue (so called danger-associated molecular patterns, “DAMPs”) as strong modulators of the systemic immune homeostasis resulting in lymphocyte apoptosis.



A) Coronal brain sections of ischemic lesions (brighter areas) with differing lesion size and location resulting in differential impact on the systemic immune system. Dot plots (below) of apoptotic T cells (PI+AnnexinV+, CD3-gated) in spleens of the respective stroke model. B) Extensive brain lesions result in splenic and thymic atrophy.



Contact: Dr. med. Arthur Liesz
Tel: +49-89-4400-46169

Feodor-Lynen-Straße 17
81377 Munich