NeuroNA Human Cellular Neuroscience Seminar // Britta Engelhardt "How the brain barriers ensure CNS immune privilege"
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Event details
Date | 26.09.2024 |
Hour | 16:00 › 17:00 |
Speaker | Britta Engelhardt, Theodor Kocher Institute, University of Bern |
Location |
Centre des Laboratoires d’Epalinges (CLE): Salle B301, and online
Online
|
Category | Conferences - Seminars |
Event Language | English |
The Human Cellular Neuroscience Seminar series, supported by the NeuroNA Foundation, informs the NeuroLéman community about progress on studies on brain development, stem cells and organoids, and mechanisms of brain and psychiatric disorders. The seminars take place alternately in Geneva at Campus Biotech (EPFL/UNIGE) and in Lausanne (CHUV/UNIL) and are also available online.
For the second seminar, we host Britta Engelhardt, who is Professor for Immunology and Director Theodor Kocher Institute at the University of Bern. Her research is devoted to understanding the function of the different brain barriers in regulating CNS immune surveillance and how their impaired function contributes to neuroinflammatory diseases such as Multiple Sclerosis (MS) or Alzheimer’s disease (AD). Her laboratory combines expertise in vascular biology, neuroimmunology and live cell imaging and has developed sophisticated in vitro and in vivo approaches to study immune cell interactions with the brain barriers in health and neuroinflammation.
Abstract
Central nervous system (CNS) neurons coordinate all our body functions by high speed electrical and chemical communication. To achieve this complex task, neurons need a strictly regulated homeostatic environment, which does not tolerate uncontrolled entry of blood components including immune cells. The CNS has thus developed a unique relationship with the immune system referred to as CNS immune privilege. The brain barriers comprise the endothelial blood-brain barrier (BBB) at the level of CNS parenchymal vessels, the epithelial blood-cerebrospinal fluid barrier (BCSFB) of the choroid plexuses (ChP) in the brain ventricles, the arachnoid barrier (AB) established by meningeal fibroblasts on the CNS surface and the evolutionary older brain barrier, the glia limitans formed by astrocytes, which encloses the entire CNS parenchyma. In our view, the brain barriers evolved for protection and defense of the CNS parenchyma analogous to the design of medieval castles surrounded by a two-walled moat. In this concept, the CNS parenchyma (castle) is protected by the outer tight junction-fortified brain barriers (BBB, BCSFB and AB) and the inner barrier constituted by the pia mater and the glia limitans. These barriers border the cerebrospinal fluid (CSF)-filled subarachnoid and perivascular spaces (castle moat) allowing for CNS immune surveillance. Under neuroinflammatory conditions immune cells cross the glia limitans and reach the CNS parenchyma leading to breakdown of CNS homeostasis and brain barrier functions. Our concept is supported by our recent observations in novel fluorescent brain barrier reporter mice that allowed for direct observation of immune cell/barrier interactions by advanced in vivo-imaging. Understanding the orchestrated function of the different brain barriers is of fundamental importance to understand how these interfaces shape CNS immunity and neuronal function and thus ultimately CNS health and disease.
For the second seminar, we host Britta Engelhardt, who is Professor for Immunology and Director Theodor Kocher Institute at the University of Bern. Her research is devoted to understanding the function of the different brain barriers in regulating CNS immune surveillance and how their impaired function contributes to neuroinflammatory diseases such as Multiple Sclerosis (MS) or Alzheimer’s disease (AD). Her laboratory combines expertise in vascular biology, neuroimmunology and live cell imaging and has developed sophisticated in vitro and in vivo approaches to study immune cell interactions with the brain barriers in health and neuroinflammation.
Abstract
Central nervous system (CNS) neurons coordinate all our body functions by high speed electrical and chemical communication. To achieve this complex task, neurons need a strictly regulated homeostatic environment, which does not tolerate uncontrolled entry of blood components including immune cells. The CNS has thus developed a unique relationship with the immune system referred to as CNS immune privilege. The brain barriers comprise the endothelial blood-brain barrier (BBB) at the level of CNS parenchymal vessels, the epithelial blood-cerebrospinal fluid barrier (BCSFB) of the choroid plexuses (ChP) in the brain ventricles, the arachnoid barrier (AB) established by meningeal fibroblasts on the CNS surface and the evolutionary older brain barrier, the glia limitans formed by astrocytes, which encloses the entire CNS parenchyma. In our view, the brain barriers evolved for protection and defense of the CNS parenchyma analogous to the design of medieval castles surrounded by a two-walled moat. In this concept, the CNS parenchyma (castle) is protected by the outer tight junction-fortified brain barriers (BBB, BCSFB and AB) and the inner barrier constituted by the pia mater and the glia limitans. These barriers border the cerebrospinal fluid (CSF)-filled subarachnoid and perivascular spaces (castle moat) allowing for CNS immune surveillance. Under neuroinflammatory conditions immune cells cross the glia limitans and reach the CNS parenchyma leading to breakdown of CNS homeostasis and brain barrier functions. Our concept is supported by our recent observations in novel fluorescent brain barrier reporter mice that allowed for direct observation of immune cell/barrier interactions by advanced in vivo-imaging. Understanding the orchestrated function of the different brain barriers is of fundamental importance to understand how these interfaces shape CNS immunity and neuronal function and thus ultimately CNS health and disease.
Links
Practical information
- Informed public
- Free
Organizer
- F. Zenk, D. Jabaudon, P. Marquet, P. Magistretti, R. Du Pasquier Host: R. Du Pasquier